Testicular toxicity of ethylene glycol monomethyl and monoethyl ethers in the rat

Foster, Paul M.D.; Creasy, Dianne M.; Foster, John R.; Thomas, Lucy V.; Cook, Melvyn W.; Gangolli, S.D.

doi:10.1016/0041-008x(83)90262-4

Cited by 175 publications

(58 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although the mechanism underlying the reproductive toxicity of EGEE is not clearly understood [10][11][12] , it has been suggested that the final metabolite, EAA, may be a determinant [13][14][15] . Differences in EAA production, therefore, may cause different degrees of damage to sperm.…”

mentioning

confidence: 99%

Reproductive Toxicity of Ethylene Glycol Monoethyl Ether in Aldh2 Knockout Mice

et al. 2007

View full text Add to dashboard Cite

Ethylene glycol monoethyl ether (EGEE) can cause damage to testes and sperm, and its metabolites are believed to play an important role in its toxicity. Aldehyde dehydrogenase 2 (ALDH2) is involved in the metabolism of this chemical. To investigate whether and how the enzyme affects the toxicity of EGEE, we conducted experiments comparing Aldh2 knockout mice with wild-type mice. Administration of EGEE at 100 and 600 mg/kg/day for one week did not induce any significant change in the weight and body weight ratios of testes, prostate and epididymides in either Aldh2 knockout or wild-type mice. However, motion of sperm from the spermaduct, as analyzed with a Hamilton-Thorne Sperm analyzer, was slightly decreased in the low dose group, and significantly lower in the high dose group; and the percentage of progressive sperm was also reduced in the two EGEE groups. This effect of EGEE treatment was observed in the wild-type, but not in the Aldh2 knockout mice. Sperm motion from the cauda epididymides was not affected. On the other hand, the concentration of ethoxyacetic acid, a metabolite of EGEE, in 24 h pooled urine of EGEE-treated Aldh2 knockout mice was not significantly lower than that of the wild-type mice on most days of urine sampling. These results suggest that inactivation of the ALDH2 enzyme due to gene mutation may be linked to differences in the susceptibility to EGEE-induced sperm toxicity.

show abstract

mentioning

confidence: 99%

Reproductive Toxicity of Ethylene Glycol Monoethyl Ether in Aldh2 Knockout Mice

et al. 2007

View full text Add to dashboard Cite

show abstract

“…EGEE and the corresponding methoxyacetic and ethoxyacetic acids have similar effects. It has been suggested that these acids are, in fact, the active metabolites (11,18) and that the injury observed is a result of zinc loss from testis, which occurs 4 days after treatment with EGME or methoxyacetic acid (18). Zinc concentration has been shown to have an important role in testicular injury induced by cadmium (19), and phthalate esters (20)(21)(22)).…”

Section: Discussionmentioning

confidence: 99%

“…There were also indications of weak dominant lethal mutation induction in mating week 8 following EGME exposure and in mating week 5 following diglyme exposure. Testicular injury caused by EGME and EGEE has been demonstrated in a number of studies (14)(15)(16)(17)(18).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Genotoxicity of Glycol Ethers

McGregor¹

1984

Environmental Health Perspectives

View full text Add to dashboard Cite

The genetic toxicology of glycol ethers is reviewed. Ethylene glycol monomethyl ether (EGME) and diglyme have been more extensively studied than other members of this series. Most results indicate a lack of genotoxic potential, but certain tests have yielded positive responses with certain compounds. Ethylene glycol monoethyl ether (EGEE) induced sister chromatid exchanges and chromosomal aberrations in cultured cells. Both EGME and diglyme induced mouse sperm head morphological changes, male rat weak dominant lethal mutations and marked, but reversible, loss of male rat fertility.

show abstract

“…The testicular toxicity of ethylene glycol monomethyl ether is the result of metabolism of the parent compound to the active toxicant, methoxyacetic acid (71). Other compounds in the class, such as ethylene glycol monobutyl ether and the propylene glycol alkyl ether series seem to be considerably less toxic to the reproductive system.…”

Section: Receptor Mechanismsmentioning

confidence: 99%

Interagency Regulatory Liaison Group Workshop on Reproductive Toxicity Risk Assessment

1986

Environmental Health Perspectives

View full text Add to dashboard Cite

Testicular toxicity of ethylene glycol monomethyl and monoethyl ethers in the rat

Cited by 175 publications

References 7 publications

Reproductive Toxicity of Ethylene Glycol Monoethyl Ether in Aldh2 Knockout Mice

Reproductive Toxicity of Ethylene Glycol Monoethyl Ether in Aldh2 Knockout Mice

Genotoxicity of Glycol Ethers

Interagency Regulatory Liaison Group Workshop on Reproductive Toxicity Risk Assessment

Contact Info

Product

Resources

About