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Additional toxicological data

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Administrative data

Endpoint:
additional toxicological information
Type of information:
migrated information: read-across from supporting substance (structural analogue or surrogate)
Adequacy of study:
supporting study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
other: see 'Remark'
Remarks:
Carbon disulphide is both a reagent in the manufacture, as well as a decomposition product of xanthates. Sodium isobutyl xanthate readily decomposes to carbon disulphide, especially in the presence of moisture/water. Therefore, the health effects of carbon disulphide (CS2) need to be considered in the assessment of sodium isobutyl xanthate.

Data source

Reference
Reference Type:
publication
Title:
Oxidation and phosphorylation processes in brain mitochondria of rats exposed to carbon disulfide.
Author:
Tarkowski S, and Sobczak H
Year:
1971
Bibliographic source:
J Neurochem 18: 177-182

Materials and methods

Type of study / information:
The effects of acute and long-term exposure to CS2, on oxidation and phosphorylation processes in brain mitochondria of rats were studied.
Test guideline
Qualifier:
no guideline followed
Principles of method if other than guideline:
The effects of acute and long-term exposure to CS2, on oxidation and phosphorylation processes in brain mitochondria of rats were studied.
GLP compliance:
not specified

Test material

Reference
Name:
Unnamed
Type:
Constituent
Test material form:
aerosol dispenser: not specified
Remarks:
migrated information: aerosol
Details on test material:
Carbon disulphide is both a reagent in the manufacture, as well as a decomposition product of xanthates. Sodium isobutyl xanthate readily decomposes to carbon disulphide, especially in the presence of moisture/water. Therefore, the health effects of carbon disulphide (CS2) need to be considered in the assessment of sodium isobutyl xanthate.
In addition, xanthates decompose on aging to form a number of byproducts, depending on the pH, temperature, etc. Risks associated with xanthate are, therefore, a function of the breakdown of the product or un-reacted raw materials remaining in the product.
- Name of test material (as cited in study report): Carbon disulfide

Results and discussion

Any other information on results incl. tables

CS2 intoxication exerted different signs of toxicity depending on the duration of treatment. After the 10-month exposure the animals experienced loss of motor equilibrium, muscular weakness, and hind-limb paresis. The acute challenging caused severe narcosis, reduced cardiac and respiratory rate, straightening of hind limbs, and lower body temperature. Nonetheless, the effects on the brain mitochondria were of the same type at both cases: disturbances in oxidative phosphorylation-uncoupling of oxidative phosphorylation, decreased phosphorus-oxygen (P:O) ratio, and a lower ATP-inorganic phosphorus (ATP-Pi) exchange rate.

Applicant's summary and conclusion

Conclusions:
CS2 poisoning (acute and chronic) to 803 and 578 ppm, respectively, resulted in similar disturbances in the brain mitochondria. The symtomps of poisoning were different for the two exposures.
Carbon disulphide is both a reagent in the manufacture, as well as a decomposition product of xanthates. Sodium isobutyl xanthate readily decomposes to carbon disulphide, especially in the presence of moisture/water. Therefore, the health effects of carbon disulphide (CS2) need to be considered in the assessment of sodium isobutyl xanthate.
Executive summary:

The effects of acute and long-term exposure to CS2, on oxidation and phosphorylation processes in brain mitochondria of rats were studied. Although rats developed different symptoms of poisoning, depending on the type of exposure, the brain mitochondria of both groups of animals exhibited the same types of disturbances in oxidative phosphorylation. The main characteristic of these disturbances was the uncoupling of oxidative phosphorylation indicated by lower respiratory control indices due to stimulation of oxidation of respiratory substrates by mitochondria in the metabolic state 4. This effect was accompanied by a decreased P:O ratio and a lower ATP-Pi exchange rate. An inhibitory effect of CS2 on the energy transfer processes is also suggested. The observed changes in oxidative phosphorylation were more distinct in the case of acute poisoning, with a longer period of an uninterrupted exposure enabling a more complete tissue saturation with CS2, than in the case of long-term exposure with shorter periods of intoxication within the day.