Sodium diethyldithiocarbamate

171.26

171.015228

205-710-6

A5304YEB5E

0446

3077

DTXSID3022956

C80963

Crystals from ethanol|Yellow to green liquid at 20 °C and 1013 hPa (solution in water)

2930909090

36.3

log Kow <1.10

Clear, colorless Liquid

1.1 g/cm³ @ Temp: 20 °C

94-96 °C

176.4°C at 760 mmHg

60.5ºC

H2O: >=10 g/100 mL at 14 ºC

Keep container tightly closed in a dry and well-ventilated place. Hygroscopic. Store under inert gas. /Sodium diethyldithiocarbamate trihydrate/

Relative vapour density (air = 1): 5.9

pKa = 2.00 (thiol) (est)

AQUEOUS SOLN IS ALKALINE TO LITMUS & PHENOLPHTHALEIN|Solubility in water = 2.9X10+4mg/L; log Kow = 1.67; VP: 0.121 mm Hg; Henry's Law constant = 6.84X10-4 atm-cu m/mol; Hydroxyl radical reaction rate constant = 2.0X10-10 cu cm/molecule-sec (all estimated at 25 °C) /Ditiocarb/|Thin, irregular plate-like crystals from acetone, mp 94-102 °C. Also reported as 90-92 °C. Freely soluble in water; soluble in ethanol, methanol, acetone. Insoluble in ether, benzene. The aqueous solution is alkaline to litmus and phenolphthalein and slowly decomposes. (pH of 10% aqueous solution is 11.6 at room temperature). The addition of an acid to the aqueous solution produces a white turbidity due to the liberation of carbon disulfide. UV max (ethanol): 257, 290 nm (epsilon 1200, 1300) /Sodium diethyldithiocarbamate trihydrate/|Greenish-yellow liquid with a characteristic smell comprising a 23% solution in water

Water soluble. Thio and dithiocarbamates slowly decompose in aqueous solution to form carbon disulfide and methylamine or other amines. Such decompositions are accelerated by acids.

Thiocarbamate Esters and Salts/Dithiocarbamate Esters and Salts

SODIUM DIETHYLDITHIOCARBAMATE is not compatible with strong oxidizing agents. Aqueous solutions slowly decompose to form carbon disulfide and an amine. Such decompositions are accelerated by acids. Addition of acid to the aqueous solution produces a white turbidity (NTP, 1992).

III

9

3077

1

EZ6475000

Dry. Well closed. Keep in a well-ventilated room. Store in an area without drain or sewer access.

Aqueous solutions decompose slowly.

P264, P270, P273, P301+P312, P330, P391, P501

H302

SRP: Expired or waste pharmaceuticals shall carefully take into consideration applicable DEA, EPA, and FDA regulations. It is not appropriate to dispose by flushing the pharmaceutical down the toilet or discarding to trash. If possible return the pharmaceutical to the manufacturer for proper disposal being careful to properly label and securely package the material. Alternatively, the waste pharmaceutical shall be labeled, securely packaged and transported by a state licensed medical waste contractor to dispose by burial in a licensed hazardous or toxic waste landfill or incinerator.|Product: Offer surplus and non-recyclable solutions to a licensed disposal company; Contaminated packaging: Dispose of as unused product. /Sodium diethyldithiocarbamate trihydrate/

Incompatible materials: Strong oxidizing agents /Sodium diethyldithiocarbamate trihydrate/

DHEW/NCI; Bioassay of Sodium Diethyldithiocarbamate for Possible Carcinogenicity (1979) Technical Rpt Series No. 172 DHEW Pub No. (NIH) 79-1728

Flash point data for this chemical are not available; however, it is probably combustible. (NTP, 1992)|Combustible. Gives off irritating or toxic fumes (or gases) in a fire.

|Warning|H302: Harmful if swallowed [Warning Acute toxicity, oral]|P264, P270, P273, P301+P312, P330, P391, and P501|P264, P270, P301+P312, P330, and P501

SMALL SPILLS AND LEAKAGE: If you spill this chemical, you should dampen the solid spill material with water, then transfer the dampened material to a suitable container. Use absorbent paper dampened with water to pick up any remaining material. Seal your contaminated clothing and the absorbent paper in a vapor-tight plastic bag for eventual disposal. Wash all contaminated surfaces with a soap and water solution. Do not reenter the contaminated area until the Safety Officer (or other responsible person) has verified that the area has been properly cleaned. STORAGE PRECAUTIONS: You should store this material under ambient temperatures and keep it away from oxidizing materials. (NTP, 1992)

RECOMMENDED RESPIRATOR: Where the neat test chemical is weighed and diluted, wear a NIOSH-approved half face respirator equipped with an organic vapor/acid gas cartridge (specific for organic vapors, HCl, acid gas and SO2) with a dust/mist filter. (NTP, 1992)|Eye/face protection: Safety glasses with side-shields conforming to EN166. Use equipment for eye protection tested and approved under appropriate government standards such as NIOSH (US) or EN 166(EU). /Sodium diethyldithiocarbamate trihydrate/|Skin protection: Handle with gloves. /Sodium diethyldithiocarbamate trihydrate/|Body Protection: Complete suit protecting against chemicals. The type of protective equipment must be selected according to the concentration and amount of the dangerous substance at the specific workplace. /Sodium diethyldithiocarbamate trihydrate/|Respiratory protection: For nuisance exposures use type P95 (US) or type P1 (EU EN 143) particle respirator. For higher level protection use type OV/AG/P99 (US) or type ABEK-P2 (EU EN 143) respirator cartridges. Use respirators and components tested and approved under appropriate government standards such as NIOSH (US) or CEN (EU). /Sodium diethyldithiocarbamate trihydrate/

Suitable extinguishing media: Use water spray, alcohol-resistant foam, dry chemical or carbon dioxide. /Sodium diethyldithiocarbamate trihydrate/|Advice for firefighters: Wear self-contained breathing apparatus for firefighting if necessary. /Sodium diethyldithiocarbamate trihydrate/

ACCIDENTAL RELEASE MEASURES: Personal precautions, protective equipment and emergency procedures: Use personal protective equipment. Avoid dust formation. Avoid breathing vapors, mist or gas. Ensure adequate ventilation. Evacuate personnel to safe areas. Avoid breathing dust; Environmental precautions: Prevent further leakage or spillage if safe to do so. Do not let product enter drains. Discharge into the environment must be avoided; Methods and materials for containment and cleaning up: Pick up and arrange disposal without creating dust. Sweep up and shovel. Keep in suitable, closed containers for disposal. /Sodium diethyldithiocarbamate trihydrate/

Precautions for safe handling: Avoid contact with skin and eyes. Avoid formation of dust and aerosols. Further processing of solid materials may result in the formation of combustible dusts. The potential for combustible dust formation should be taken into consideration before additional processing occurs. Provide appropriate exhaust ventilation at places where dust is formed. /Sodium diethyldithiocarbamate trihydrate/|Appropriate engineering controls: Handle in accordance with good industrial hygiene and safety practice. Wash hands before breaks and at the end of workday. /Sodium diethyldithiocarbamate trihydrate/|Gloves must be inspected prior to use. Use proper glove removal technique (without touching glove's outer surface) to avoid skin contact with this product. Dispose of contaminated gloves after use in accordance with applicable laws and good laboratory practices. Wash and dry hands. /Sodium diethyldithiocarbamate trihydrate/|SRP: Local exhaust ventilation should be applied wherever there is an incidence of point source emissions or dispersion of regulated contaminants in the work area. Ventilation control of the contaminant as close to its point of generation is both the most economical and safest method to minimize personnel exposure to airborne contaminants. Ensure that the local ventilation moves the contaminant away from the worker.

Do NOT let this chemical enter the environment. Sweep spilled substance into covered containers. If appropriate, moisten first to prevent dusting. Carefully collect remainder. Then store and dispose of according to local regulations.

Dry. Well closed. Keep in a well-ventilated room. Store in an area without drain or sewer access.

Evaporation at 20 °C is negligible; a nuisance-causing concentration of airborne particles can, however, be reached quickly when dispersed.

The substance is irritating to the skin, eyes and upper respiratory tract.

NO open flames.

Use local exhaust.

Protective gloves.

Wear safety spectacles.

According to the 2012 TSCA Inventory Update Reporting data, one reporting facility stated that the number of persons reasonably likely to be exposed during the manufacturing, processing, or use of sodium diethyditiocarbamate in the United States may be confidential business information (CBI)(1).

IDENTIFICATION AND USE: Sodium diethyldithiocarbamate (DETC) is a solid. It is used as corrosive inhibitor, rubber accelerator, intermediate, polymerization shortstop, and chemical intermediate in production of bis(thiocarbamoyl)sulfides (rubber-processing accelerators and fungicides). It is also used for colorimetric determination of small quantities of copper and for its separation from other metals, as well as spin trap (as FeDETC complex) for nitric oxide detection. DETC has also been used as a medication and antidote in nickel carbonyl exposures. HUMAN EXPOSURE AND TOXICITY: Allergic contact dermatitis from a wet suit was related to zinc diethyldithiocarbamate. ANIMAL STUDIES: Zinc diethyldithiocarbamate and DETC were positive in the murine local lymph node assay (LLNA). Administered systemically, DETC is reported to have caused detachment of the retina in dogs, but no damage to the retina in monkeys. In albino rats and beagle dogs, it caused no impairment of vision or structural alteration in the eye after daily administration for ninety days. In a 6-wk experiment in mice, daily sc injection of 50 mg/kg bw had marked anti-thyroid activity. DETC administered to rabbits at 100, 200, and 400 mg/kg daily for 4 weeks increased triglyceride and phospholipid levels. No changes were found in serum cholesterol concentration. DETC reduces blood copper concentrations. Pregnant rabbits injected intravenously with 0.5 g sodium diethyldithiocarbamate/day on 5 days per week throughout pregnancy failed to deliver litters. DETC elevated copper levels in the brain and peripheral nerve, leading to oxidative stress and lipid peroxidation from redox cycling of copper. Lipid peroxidation appears to either be a contributing event in the development of demyelination, possibly through an increase of redox active copper, or a consequence of the myelin injury. Continued DETC exposure induced an extensive degeneration of axons and myelin sheath (Wallerian degeneration in axons). DETC was not carcinogenic to rats or mice in NTP bioassay. Sodium diethyldithiocarbamate was negative when tested using Salmonella typhimurium strains (TA1535, TA1537, TA97, TA98 and TA100) in the presence and absence of metabolic activation. However, a small but significant increase in the number of chromosome breakages and aberrations was found in Vicia faba. DETC given orally to young and adult domestic fowl produced retarded testicular development, and produced degeneration in the seminiferous epithelium of mature birds. Nerve fiber degeneration was produced in the medulla and spinal cord of chicks. ECOTOXICITY STUDIES: DETC>3 mg/L applied to developing frog embryos was lethal in 24 hr. Between 1-3 mg/L caused severely malformed embryos. Retardation of growth, curvature of body axis, general edemic condition, pigmentation disorders, and abnormal notochords were noted.

Rats exposed to enflurane (100 ppm) or methoxyflurane (300 ppm) in a closed all glass system eliminated these anesthetics from atmosphere with half life of 6.84 hr for enflurane and 0.64 for methoxyflurane. Pretreatment with dithiocarb (100 mg/kg ip) prolonged elimination half life of both compounds.|Rat liver microsomes catalyze covalent binding of (14)C-carbon tetrachloride metabolites to the microsomal protein; this binding was inhibited by dithiocarb at an I50 (50% inhibition) of 2.3x10-5 moles. Dithiocarb effectively inhibited metabolic elimination of carbon tetrachloride at a dose of 100 mg/kg.|Dithiocarb increased T-cell associated responses in mice treated with azathioprine or hydrocortisone acetate. Such a beneficiary effect contrasted with its inefficiency to restore functions abrogated by cyclophosphamide. The results raise the possibility of developing a rational chemoimmunotherapy using dithiocarb with a compatible cytoreductive drug.|Sc injection of 0.5 mmoles dithiocarb, 30 min before an ip injection of 280 mg aniline- hydrocloric acid/kg, affected aniline toxicity to rats by increasing mortality from 41.6 to 75%, decreasing methemoglobin formation by 67.72%, and inhibiting hepatic aniline hydroxylase by 47.6%.|For more Interactions (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (15 total), please visit the HSDB record page.

LD50 Rat oral 2830 mg/kg /Trihydrate/|LD50 Mouse oral 1870 mg/kg /Trihydrate/|LD50 Mouse iv >1000 mg/kg /Trihydrate/|LD50 Rat oral 1500 mg/kg|For more Non-Human Toxicity Values (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (8 total), please visit the HSDB record page.

/AQUATIC SPECIES/ The effects of intraperitoneal injection of diethyldithiocarbamate (DDC) on free radical processes were examined in brain, liver and kidney of goldfish (Carassius auratus). Levels of oxidatively modified lipids and proteins as well as the activities of antioxidant and associated enzymes were measured. Intraperitoneal injection of DDC at a concentration of 0.01 mg/g wet mass decreased SOD activities by about 30-50% after 48 and 168 hr compared to corresponding sham-injected values. This treatment resulted in transient oxidative stress. Lipid peroxide content increased after DDC injection at all time points in the kidney, after 48 hr in the liver and was elevated in most experimental groups in the brain. Thiobarbituric-acid reactive substances (end products of lipid peroxidation) rose within the first 48 hr after injection, but returned to initial levels after 168 hr. Two other indices of oxidative stress were also transiently modified: protein carbonyl levels in the brain and kidney increased 24 hr post-injection, and the low-molecular mass thiol content was reduced over the same period in all tissues examined. Activities of catalase, glutathione peroxidase, glutathione-S-transferase, glutathione reductase, and glucose-6-phosphate dehydrogenase showed differential responses to DDC treatment that rebounded by 168 hr post-injection. Glutathione peroxidase activities were reduced by 60, 45 and 65% in the brain, liver and kidney, respectively, after 24 hr but rebounded thereafter. After 48 hr post-injection with DDC significant decreases were also seen in liver and kidney catalase, GST activities in all three tissues, and kidney GR and G6PDH activities. In some cases, catalase, GST, GR and G6PDH activities transiently increased after 24 hr. It was concluded that DDC injection depleted SOD and simultaneously stimulated lipid peroxidation, but did not require compensatory enhancement of other enzymatic defenses. Different actions of the superoxide anion in cellular metabolism and possible consequences of the impairment of superoxide dismutase are discussed.|/AQUATIC SPECIES/ Sodium diethyldithiocarbamate concentration >3 mg/L applied to developing frog embryos were lethal in 24 hr. Between 1-3 mg/L caused severely malformed embryos. Retardation of growth, curvature of body axis, general edemic condition, pigmentation disorders, and abnormal notochords were noted.

A bioassay of sodium diethyldithiocarbamate for possible carcinogenicity was conducted by admin the test chemical in feed to F344 rats and B6C3Fl mice. Groups of 50 rats of each sex were admin sodium diethyldithiocarbamate at one of two doses, either 1,250 or 2,500 ppm, for 104 wk. Groups of 50 mice of each sex were admin sodium diethyldithiocarbamate at one of two doses, either 500 or 4,000 ppm, for 108 or 109 wk. Matched controls consisted of 16 untreated male rats, 20 untreated female rats and 20 untreated mice of each sex. All surviving rats and mice were /sacrificed/ at the end of administration of the test chemical. ... It is concluded that under the conditions of this bioassay, sodium diethyldithiocarbamate was not carcinogenic for F344 rats or B6C3Fl mice of either sex. ... Levels of Evidence of Carcinogenicity: Male Rats: Negative; Female Rats: Negative; Male Mice: Negative; Female Mice: Negative.

Sodium diethyldithiocarbamate is not known to occur as a natural product.

Sodium diethyldithiocarbamate's production and use in colorimetric determination of small quantities of copper and for its separation from other metals(1,2) and experimental administration as a trial HIV drug(3) will result in its release to the environment through various waste streams(SRC).

Sodium diethyldithiocarbamate may undergo hydrolysis in soils, though no quantitative estimate of the rate of this reaction was made.|Sodium diethyldithiocarbamate was found to be stable in aqueous solution at pH 7 but decomposed under slightly acidic conditions (pH 5-6.7), producing carbon disulfide and a salt of diethylamine.

NIOSH (NOES Survey 1981-1983) has statistically estimated that 7,970 workers (1,982 of these are female) are potentially exposed to sodium diethyldithiocarbamate in the US(1).

Adjuvants, Immunologic; Antiviral Agents; Chelating Agents|/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Sodium Diethyldithiocarbamate is included in the database.|/EXPL THER/ A brief historical resume is presented on the use of dithiocarbamates for the treatment of persons exposed to nickel carbonyl. The specificity of the treatment is demonstrated in an industrial accident in which four men were simultaneously exposed to nickel carbonyl vapors. Three of the men received dithiocarb within 24 hours after exposure and the fourth was hospitalized by his family physician and treated for bronchopneumonia with antibiotics and without benefit of dithiocarb. The three workmen who received dithiocarb became symptomless and returned to work within 72 hours after exposure. The fourth man who had not received dithiocarb died within five days after exposure.|/EXPL THER/ We randomized 389 symptomatic patients with human immunodeficiency virus (HIV) infection to ditiocarb sodium (400 mg/cu m orally for 24 weeks) or a placebo. Patients were well balanced according to Centers for Disease Control (CDC) group, CD4+ cell number, and duration of disease prior to entry. Ten new acquired immunodeficiency syndrome (AIDS)-defining opportunistic infections occurred in the treated patients and 21 in the controls. Reduction of new opportunistic infections in the ditiocarb group was significant in all patients (relative risk [RR], 0.44) and in patients with AIDS (CDC groups IV-C1 and IV-D) (RR, 0.12). The size of the effect of ditiocarb was maintained when data were reanalyzed after exclusion of a patient who progressed to Pneumocystis carinii pneumonia who was not strictly CDC-defined (RR, 0.46), or when considering as new opportunistic infections three events, which were clinically active at entry, but for which the definitive diagnosis was made during study (RR, 0.49). The administration of ditiocarb did not induce any major adverse clinical or biological reactions. We conclude that, in this study, ditiocarb was safe and reduced the incidence of opportunistic infections in patients with symptomatic HIV infection.|For more Therapeutic Uses (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (10 total), please visit the HSDB record page.

Chemicals that bind to and remove ions from solutions. Many chelating agents function through the formation of COORDINATION COMPLEXES with METALS. (See all compounds classified as Chelating Agents.)|Substances that augment, stimulate, activate, potentiate, or modulate the immune response at either the cellular or humoral level. The classical agents (Freund's adjuvant, BCG, Corynebacterium parvum, et al.) contain bacterial antigens. Some are endogenous (e.g., histamine, interferon, transfer factor, tuftsin, interleukin-1). Their mode of action is either non-specific, resulting in increased immune responsiveness to a wide variety of antigens, or antigen-specific, i.e., affecting a restricted type of immune response to a narrow group of antigens. The therapeutic efficacy of many biological response modifiers is related to their antigen-specific immunoadjuvanticity. (See all compounds classified as Adjuvants, Immunologic.)|Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly. (See all compounds classified as Antiviral Agents.)

Rats receiving levels of 500 mg of dithiocarb in 1-2 mL water/kg body weight by gavage reached plasma levels of 2 mg/L dithiocarb in 3 hours.|A half life for absorption of 26 minutes was determined when S-dithiocarb dissolved in 2M phosphate buffer was injected into the small intestinal lumen of adult male Wistar rats at a dose of 25 mg/kg.|Within 15 minutes of dosing rats with 25 mg (222 moles S)/rat S-dithiocarb i.p., nonprotein bound radiolabel was detected in the plasma (1561 nmoles/mL plasma) and in the liver (3211 nmoles/g liver). A substantial amount (>45% within 15 minutes of dosing) of radioactivity also was found to be bound reversibly to soluble proteins of liver and plasma.|A small amount (<0.1%) of unchanged dithiocarb was detected in the urine of rats receiving ip injections of 25 mg (35)S-dithiocarb/rat. One hr after dosing, 96.1% of the radiolabeled urinary metabolites was of S-glucuronide conjugate and 3.9% inorganic sulfate. Within 1 hr after dosing, 7% of the administered (35)S-dithiocarb was recovered as carbon disulfide in the expired air.|For more Absorption, Distribution and Excretion (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (7 total), please visit the HSDB record page.

In rats, four metabolites, diethyldithiocarbamate, diethyldithiocarbamate-s-glucuronide, inorganic sulfate and carbon disulfide were identified; these are also metabolites of disulfiram.

Although the ability of disulfiram to inactivate CYP2E1 has been known for more than 20 years, the mechanism has not yet been elucidated. A metabolite of disulfiram, diethyldithocarbamate (DDC), is converted by CYP2E1 to a reactive intermediate that subsequently inactivates the protein, leading to mechanism-based inactivation. Mass spectral analysis of the inactivated human 2E1 protein demonstrates that the inactivation is due to the formation of an adduct of the reactive metabolite of DDC with the apoprotein. These data, along with mass spectral analysis of a reactive intermediate trapped with GSH, indicate the involvement of a reactive intermediate with a molecular mass of 116 Da. Our results suggest that this binding involves formation of a disulfide bond with one of the eight cysteines in CYP2E1. The inactivation of wild-type CYP2E1 as well as two of its polymorphic mutants, CYP2E1*2 and CYP2E1*4, was also investigated. For wild-type CYP2E1, the K(I) was 12.2 uM and the k(inact) was 0.02 min(-1). The K(I) values for the two polymorphic mutants were 227.6 and 12.4 uM for CYP2E1.2 and CYP2E1.4, and the k(inact) values were 0.0061 and 0.0187 min(-1), respectively. These data indicate that DDC is a much less efficient inactivator of CYP2E1.2 than it is of either the wild-type or the CYP2E1.4 variant.|... DDTC significantly inhibited the activity of superoxide dismutase and the activity of gamma-glutamyl transpeptidase, glutathione reductase, and alkaline phosphatase, whereas an increase in the activity of glutathione peroxidase was found. The membranes of pneumocytes type II were injured.

SYMPTOMS: Symptoms of exposure to this chemical include irritation of the eyes. Continued exposure may cause mild skin irritation. The dusts of this compound are caustic to the mucous membranes. This compound is also caustic to the digestive tract. ACUTE/CHRONIC HAZARDS: This chemical may be harmful if swallowed or inhaled. When heated to decomposition it emits very toxic fumes of nitrogen oxides, sulfur oxides and sodium oxide. (NTP, 1992)

EYES: First check the victim for contact lenses and remove if present. Flush victim's eyes with water or normal saline solution for 20 to 30 minutes while simultaneously calling a hospital or poison control center. Do not put any ointments, oils, or medication in the victim's eyes without specific instructions from a physician. IMMEDIATELY transport the victim after flushing eyes to a hospital even if no symptoms (such as redness or irritation) develop. SKIN: IMMEDIATELY flood affected skin with water while removing and isolating all contaminated clothing. Gently wash all affected skin areas thoroughly with soap and water. If symptoms such as redness or irritation develop, IMMEDIATELY call a physician and be prepared to transport the victim to a hospital for treatment. INHALATION: IMMEDIATELY leave the contaminated area; take deep breaths of fresh air. If symptoms (such as wheezing, coughing, shortness of breath, or burning in the mouth, throat, or chest) develop, call a physician and be prepared to transport the victim to a hospital. Provide proper respiratory protection to rescuers entering an unknown atmosphere. Whenever possible, Self-Contained Breathing Apparatus (SCBA) should be used; if not available, use a level of protection greater than or equal to that advised under Protective Clothing. INGESTION: DO NOT INDUCE VOMITING. If the victim is conscious and not convulsing, give 1 or 2 glasses of water to dilute the chemical and IMMEDIATELY call a hospital or poison control center. Be prepared to transport the victim to a hospital if advised by a physician. If the victim is convulsing or unconscious, do not give anything by mouth, ensure that the victim's airway is open and lay the victim on his/her side with the head lower than the body. DO NOT INDUCE VOMITING. IMMEDIATELY transport the victim to a hospital. (NTP, 1992)

Fresh air, rest.

Remove contaminated clothes. Rinse skin with plenty of water or shower.

First rinse with plenty of water for several minutes (remove contact lenses if easily possible), then refer for medical attention.

Immediate first aid: Ensure that adequate decontamination has been carried out. If patient is not breathing, start artificial respiration, preferably with a demand valve resuscitator, bag-valve-mask device, or pocket mask, as trained. Perform CPR if necessary. Immediately flush contaminated eyes with gently flowing water. Do not induce vomiting. If vomiting occurs, lean patient forward or place on left side (head-down position, if possible) to maintain an open airway and prevent aspiration. Keep patient quiet and maintain normal body temperature. Obtain medical attention. /Poisons A and B/|Basic treatment: Establish a patent airway (oropharyngeal or nasopharyngeal airway, if needed). Suction if necessary. Watch for signs of respiratory insufficiency and assist ventilations if needed. Administer oxygen by nonrebreather mask at 10 to 15 L/min. Monitor for pulmonary edema and treat if necessary ... . Monitor for shock and treat if necessary ... . Anticipate seizures and treat if necessary ... . For eye contamination, flush eyes immediately with water. Irrigate each eye continuously with 0.9% saline (NS) during transport ... . Do not use emetics. For ingestion, rinse mouth and administer 5 mL/kg up to 200 mL of water for dilution if the patient can swallow, has a strong gag reflex, and does not drool ... . Cover skin burns with dry sterile dressings after decontamination ... . /Poisons A and B/|Advanced treatment: Consider orotracheal or nasotracheal intubation for airway control in the patient who is unconscious, has severe pulmonary edema, or is in severe respiratory distress. Positive-pressure ventilation techniques with a bag-valve-mask device may be beneficial. Consider drug therapy for pulmonary edema ... . Consider administering a beta agonist such as albuterol for severe bronchospasm ... . Monitor cardiac rhythm and treat arrhythmias as necessary ... . Start IV administration of D5W TKO. Use 0.9% saline (NS) or lactated Ringer's (LR) if signs of hypovolemia are present. For hypotension with signs of hypovolemia, administer fluid cautiously. Watch for signs of fluid overload ... . Treat seizures with diazepam (Valium) or lorazepam (Ativan) ... . Use proparacaine hydrochloride to assist eye irrigation ... . /Poisons A and B/

/CASE REPORTS/ Rubber materials are common causes of contact dermatitis. Neoprene is a special synthetic rubber used in many products (eg, wet suits, elastic supports, gloves, shoes, and orthopedic devices). A 31-year-old man was admitted to our dermatoallergologic clinic with the development of a generalized itching erythematovesicular eruption. He reported that clinical manifestations occurred after he wore a neoprene wet suit that he was used to wearing for water sports. Although allergic contact dermatitis from a wet suit is not uncommon, it is usually due to thiourea derivatives whereas our patient presented with contact allergy to p-tert-butylphenol formaldehyde resin and zinc diethyldithiocarbamate. /Zinc diethyldithiocarbamate/|/ALTERNATIVE and IN VITRO TESTS/ Tumor necrosis factor-alpha (TNF-alpha) and etoposide both trigger a large and rapid production of reactive oxygen species (ROS) in HeLa cells. This occurs before translocations of the proapoptotic Bax and cytochrome c proteins, the loss of mitochondrial membrane potential (DeltaPsim), and apoptosis. We have used diethyldithiocarbamate (DDC), a well-known inhibitor of Cu, Zn superoxide dismutase to study the role of ROS in this system. We report that DDC strongly inhibits caspase activation, loss of DeltaPsim, and cell death induced by TNF-alpha or etoposide. Surprisingly, DDC does not inhibit Bax and cytochrome c translocations. On the contrary, we have observed that DDC can trigger the translocations of these proteins by itself, without altering DeltaPsim. Here, we report that DDC has at least two antagonistic apoptosis regulation functions. First, DDC triggers ROS-dependent Bax and cytochrome c translocations, which are potentially proapoptotic, and second, DDC inhibits caspase activation and activity, loss of DeltaPsim, and cell death, in a ROS-independent manner. Our results suggest an interesting model in which ROS-dependent Bax and cytochrome c translocations can be studied without interference from later apoptotic events.|/ALTERNATIVE and IN VITRO TESTS/ Antimycin A (AMA) inhibits mitochondrial electron transport between cytochrome b and c. We recently demonstrated that AMA inhibits the growth of lung cancer Calu-6 cells and the changes of reactive oxygen species (ROS) and glutathione (GSH) levels affect apoptosis in Calu-6 cells. Here, we examined the effects of N-acetyl-cysteine (NAC, a well known antioxidant), L-buthionine sulfoximine (BSO, an inhibitor of GSH synthesis), diethyl-dithiocarbamate (DDC, an inhibitor of Cu, Zn-SOD) or 3-amino-1,2,4-triazole (AT, an inhibitor of catalase) on AMA-treated Calu-6 cells in relation to cell death, ROS and GSH levels. Treatment with AMA induced cell growth inhibition, apoptosis and the loss of mitochondrial membrane potential (MMP) (DeltaPsim) in Calu-6 cells. While the intracellular ROS level was decreased in 50 microM AMA-treated Calu-6 cells, O2.- levels among ROS were significantly increased. AMA also induced GSH depletion in Calu-6 cells. Treatment with NAC showed decreasing effect on O2.- levels in AMA-treated cells preventing apoptosis, MMP (DeltaPsim) loss and GSH depletion in these cells. BSO significantly increased GSH depletion and apoptosis in AMA-treated cells. While both DDC and AT increased ROS levels in AMA-treated Calu-6 cells, only DDC intensified GSH depletion and apoptosis. BSO and AT increased the ROS level in Calu-6 control cells, but these agents did not induce apoptosis and GSH depletion. In conclusion, our results suggest that GSH depletion rather than ROS level in AMA-treated Calu-6 cells is more tightly related to apoptosis.|/ALTERNATIVE and IN VITRO TESTS/ Propyl gallate (PG) as a synthetic antioxidant is widely used in processed food and medicinal preparations. It also exerts a variety of effects on tissue and cell functions. In the present study, we investigated the effects of L-buthionine sulfoximine (BSO, an inhibitor of GSH synthesis), diethyldithiocarbamate (DDC, an inhibitor of Cu/Zn-SOD) or 3-amino-1,2,4-triazole (AT, an inhibitor of catalase) on PG-treated HeLa cells in relation to cell growth, reactive oxygen species (ROS) and glutathione (GSH). Treatment with PG induced growth inhibition, the loss of mitochondrial membrane potential [MMP (DeltaPsim)] and apoptosis in HeLa cells. ROS levels including O2.- were increased or decreased in PG-treated HeLa cells depending on the incubation times. PG caused depletion in GSH content in HeLa cells. While BSO enhanced the growth inhibition of PG-treated HeLa cells at 4 hr, DDC and AT did not. All the agents down-regulated MMP (DeltaPsim) levels in PG-treated cells. Although BSO, DDC or AT slightly increased ROS or O2.- levels in PG-treated cells at 1 hr, these enhancements of ROS did not intensify apoptosis in these cells. In addition, BSO, DDC or AT slightly reduced GSH level in PG-treated HeLa cells at 1 hr, but this reduction did not affect cell death of HeLa. Furthermore, PG induced a G1 phase arrest of the cell cycle. BSO, DDC or AT significantly inhibited the G1 phase arrest in PG-treated cells. Conclusively, the changes of ROS and GSH levels by BSO, DDC or AT in PG-treated HeLa cells did not strongly affect the cell growth and death.|For more Human Toxicity Excerpts (Complete) data for SODIUM DIETHYLDITHIOCARBAMATE (7 total), please visit the HSDB record page.

Ammonium Salt Ditiocarb

The substance can be absorbed into the body by ingestion.

Cough. Sore throat.

Redness.

Redness.

Utilities|Carbamodithioic acid, N,N-diethyl-, sodium salt (1:1): ACTIVE|Sodium diethyldithiocarbamate is available in the US for use in rubber processing as a 25% active aqueous solution... .

The mechanism of NO trapping by iron-diethylthiocarbamate complexes was investigated in cultured cells and animal and plant tissues. Contrary to common belief, the NO radicals are trapped by iron-diethylthiocarbamates not only in ferrous but in ferric state also in the biosystems. When DETC was excess over endogenous iron ligands like citrate, ferric DETC complexes were directly observed with EPR spectroscopy at g=4.3. This was the case when isolated spinach leaves, endothelial cultured cells were incubated in the medium with 2.5 mM DETC or mouse liver was perfused with 100 mM DETC solution. After trapping NO, the nitrosylated Fe-DETC adducts are mostly in diamagnetic ferric state, with only a minor fraction having been reduced to paramagnetic ferrous state by endogenous biological reductants. In actual in vivo trapping experiments with mice, the condition of excess DETC was not met. The substantial quantities of iron in animal tissues were bound to ligands other than DETC, in particular citrate. These non-DETC complexes appear as roughly equal mixtures of ferric and ferrous iron. The presence of NO favors the replacement of non-DETC ligands by DETC. In all biological systems considered here, the nitrosylated Fe-DETC adducts appear as mixture of diamagnetic and paramagnetic states. The diamagnetic ferric nitrosyl complexes may be reduced ex vivo to paramagnetic form by exogenous reductants like dithionite. The trapping yields are significantly enhanced upon exogenous reduction, as proven by NO trapping experiments in plants, cell cultures and mice.|A simple high-performance liquid chromatography method is adopted in order to quantitate the amount of zinc diethyldithiocarbamate (ZDEC) released into artificial sweat from natural rubber latex vulcanizates. The artificial sweat is extracted with dichloromethane, and the residue is recovered and re-dissolved in a known quantity of dichloromethane. ZDEC is quantitated as its copper complex by reacting with copper(II) sulphate. A reversed-phase C18 column and detection wavelength of 435 nm are used to measure the copper-dithiocarbamate complex. The procedure is repeated with cobalt(II) chloride, and the amount of ZDEC obtained by both the methods is compared. It is found that the recovery of ZDEC from the artificial sweat is high when copper(II) sulphate is used, indicating that the copper(II) sulphate is a better complexing agent than cobalt(II) chloride under the conditions used in the present study. The limits of detection and the quantitation of ZDEC are found to be 0.25 and 0.86 ug/mL, respectively. The present method, based on precolumn derivatization using copper(II) sulphate, facilitates the quantitation of ZDEC in latex products.|Concentrations of 5X10-5 to 5X10-4 M dithiocarbamates have been analyzed by direct current polarographic methods in which anodic waves correspond to the formation of mercury compounds: Halls DJ et al; Analyt Chim Acta 41: 51-62 (1968); when short, controlled drop times are used, concentrations of 1.6X10-3 molar can be determined by this method: Canterford DR et al; Analyt Chem 45: 1327-31 (1973). The application of differential pulse polarography has increased the sensitivity of the method to a detection limit of 1X10-6 molar & a quantitiative limit of 2X10-6 M: Canterford DR, Buchanan AS; Electroanalyt Chem Interfacial Electrochem 44: 291-8 (1973).|Sodium diethyldithiocarbamate can be determined by titration of the excess iodine solution resulting from the sodium diethyldithiocarbamate-induced iodine-azide reaction. The range which could be determined was from 5-160 ug in 50 or 100 cu cm of solution, with a relative error of +/- 3%.|A gas chromatographic method for determining N,N-dialkyl dithiocarbamates (fungicide, vulcanization, accelerators, antioxidant) iN industrial wastewater at the ng level is described. The sample is freeze-dried, extracted with ethanol & then esterified with 1-iodopropane. Sensitivity of the method is about 1 ng. /Sodium N,N-dialkyl dithiocarbamates and their S-N-propyl esters/