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Epididymal GSH in Chemical-Induced Germ Cell Mutations.

PB89152607

Publication Date	1988
Personal Author	Gandy, J.
Page Count	32
Abstract	The effect of changing concentrations of glutathione (GSH) in the male reproductive tract was investigated using mature rats sacrificed following administration of various test compounds selected for their ability to perturb GSH levels. GSH content was determined in the liver, testes, and epididymides. GSH levels in all tested organs were significantly reduced following administration of isophorone (500 mg/kg), phorone (250 mg/kg), and diethylmaleate (500 mg/kg). Isophorone treatment resulted in a significantly enhanced binding of tritium labeled ethyl-methanesulfonate (3H-EMS) to sperm heads. Hepatic and epididymal GSH was reduced following trimethyl-phosphate (600 mg/kg), naphthalene (500 mg/kg) and methyl-iodide (100 mg/kg) administration, but no change was noted in testicular levels. The authors suggest that chemically induced lowering of GSH in the male reproductive tract may be a mechanism for potentiation of chemically induced germ cell mutations. Subsequent tests indicated that treatment with acivicin plus N-acetyl-cysteine served to enhance the levels of GSH in reproductive tissue in-vivo. Studies are being conducted to determine whether this increase will offer protection against the mutagenic effects of ethyl-methanesulfonate.
Keywords	Toxicity Glutathione Reproduction(Biology) Laboratory animals Rats Germ cells Mutations Coenzymes Males Iodides Naphthalene compounds Occupational safety and health Fetal death CAS 78-59-1 CAS 504-20-1 CAS 512-56-1 CAS 91-20-3 CAS 74-88-4 CAS 87-86-5 CAS 103-90-2
Source Agency	National Institute for Occupational Safety and Health
NTIS Subject Category	57Y - Toxicology 57Q - Pharmacology & Pharmacological Chemistry 57O - Pathology
Corporate Authors	Arkansas Univ. for Medical Sciences, Little Rock.; National Inst. for Occupational Safety and Health, Cincinnati, OH.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Cincinnati, OH.
Document Type	Technical Report
Title Note	Final rept.,
NTIS Issue Number	198911

Epididymal GSH in Chemical-Induced Germ Cell Mutations.

Epididymal GSH in Chemical-Induced Germ Cell Mutations.
PB89152607

Publication Date	1988
Personal Author	Gandy, J.
Page Count	32
Abstract	The effect of changing concentrations of glutathione (GSH) in the male reproductive tract was investigated using mature rats sacrificed following administration of various test compounds selected for their ability to perturb GSH levels. GSH content was determined in the liver, testes, and epididymides. GSH levels in all tested organs were significantly reduced following administration of isophorone (500 mg/kg), phorone (250 mg/kg), and diethylmaleate (500 mg/kg). Isophorone treatment resulted in a significantly enhanced binding of tritium labeled ethyl-methanesulfonate (3H-EMS) to sperm heads. Hepatic and epididymal GSH was reduced following trimethyl-phosphate (600 mg/kg), naphthalene (500 mg/kg) and methyl-iodide (100 mg/kg) administration, but no change was noted in testicular levels. The authors suggest that chemically induced lowering of GSH in the male reproductive tract may be a mechanism for potentiation of chemically induced germ cell mutations. Subsequent tests indicated that treatment with acivicin plus N-acetyl-cysteine served to enhance the levels of GSH in reproductive tissue in-vivo. Studies are being conducted to determine whether this increase will offer protection against the mutagenic effects of ethyl-methanesulfonate.
Keywords	Toxicity Glutathione Reproduction(Biology) Laboratory animals Rats Germ cells Mutations Coenzymes Males Iodides Naphthalene compounds Occupational safety and health Fetal death CAS 78-59-1 CAS 504-20-1 CAS 512-56-1 CAS 91-20-3 CAS 74-88-4 CAS 87-86-5 CAS 103-90-2
Source Agency	National Institute for Occupational Safety and Health
NTIS Subject Category	57Y - Toxicology 57Q - Pharmacology & Pharmacological Chemistry 57O - Pathology
Corporate Authors	Arkansas Univ. for Medical Sciences, Little Rock.; National Inst. for Occupational Safety and Health, Cincinnati, OH.
Supplemental Notes	Sponsored by National Inst. for Occupational Safety and Health, Cincinnati, OH.
Document Type	Technical Report
Title Note	Final rept.,
NTIS Issue Number	198911