Disease relevance of 4-vinylcyclohexene

• Here we show that Nrf2 protects against the ovarian toxicity of 4-vinylcyclohexene diepoxide (VCD) in mice [1].

High impact information on 4-vinylcyclohexene

• Bax, caspase-2, and caspase-3 are required for ovarian follicle loss caused by 4-vinylcyclohexene diepoxide exposure of female mice in vivo [2].
• The industrial chemical, 4-vinylcyclohexene diepoxide (VCD), kills oocytes within immature follicles in the ovaries of mice and rats and is considered a potential occupational health hazard [2].
• Repeated dosing with 4-vinylcyclohexene diepoxide (VCD) accelerates atresia via apoptosis in primordial and primary follicles in ovaries of rats [3].
• Mice but not rats are susceptible to 4-vinylcyclohexene (VCH)-induced ovarian toxicity and carcinogenicity [4].
• The stereochemical course of the biotransformation of 1,2-monoepoxides of 4-vinylcyclohexene (2 and 3) by liver microsomes from control and induced rats and by purified P4502B1 and P4502E1 has been determined [5].

Biological context of 4-vinylcyclohexene

• The stereochemical course of the biotransformation of 4-vinylcyclohexene (VCH, 1) by liver microsomes from male and female control and induced rats and purified rat P450 2B1 and 2E1 has been determined [6].
• The metabolites, cis- and trans-4-vinylcyclohexene 1,2-epoxide (2 and 3, respectively) and the isomeric 4-vinylcyclohexene 7,8-epoxides (4 and 5), were rapidly biotransformed into the corresponding vicinal diols by mEH-catalyzed hydrolysis [6].
• Rats are exposed to repeated daily dosing (20 days) with 4-vinylcyclohexene diepoxide (VCD) to cause early ovarian failure (model for postmenopause), and ovaries are directly exposed to 7,12-dimethylbenz(a)anthracene (DMBA) to cause abnormal ovarian proliferation and neoplasia [7].
• Repeated dosing of rats with the ovotoxic chemical, 4-vinylcyclohexene diepoxide (VCD), destroys primordial and primary ovarian follicles via apoptosis (physiological cell death) by accelerating the normal rate of atresia [8].
• OBJECTIVE: To determine whether the 4-vinylcyclohexene diepoxide (VCD)-treated mouse menopause model, which involves accelerated atresia of primordial follicles and induces gradual ovarian failure (while sparing the ovarian stroma), can be adapted to nonhuman primates [9].

Anatomical context of 4-vinylcyclohexene

• Stereochemical aspects in the 4-vinylcyclohexene biotransformation with rat liver microsomes and purified p450s. monoepoxides and diols [6].
• Epoxidation of 4-vinylcyclohexene by human hepatic microsomes [10].
• Effect of 4-vinylcyclohexene on micronucleus formation in the bone marrow of rats and mice [11].

Associations of 4-vinylcyclohexene with other chemical compounds

• Carcinogencity bioassays of bisphenol A, 4-vinylcyclohexene diepoxide, and 4-vinycyclohexene [12].

Gene context of 4-vinylcyclohexene

• Activation of mitogen-activated protein kinases and AP-1 transcription factor in ovotoxicity induced by 4-vinylcyclohexene diepoxide in rats [13].
• Apoptosis induced in rats by 4-vinylcyclohexene diepoxide is associated with activation of the caspase cascades [14].
• Role of induction of specific hepatic cytochrome P450 isoforms in epoxidation of 4-vinylcyclohexene [15].
• This enantiomer is also formed as nearly the sole product by P450-catalyzed epoxidation of (1R,2S,4R)-trans-3b, the monoepoxide that, as a consequence of the selective formation from 4-vinylcyclohexene and/or reduced elimination by epoxide hydrolase, tends to accumulate in rat [5].
• Induction of cytochrome P-450 enzymes after repeated exposure to 4-vinylcyclohexene in B6C3F1 mice [16].

Analytical, diagnostic and therapeutic context of 4-vinylcyclohexene

• Toxicological evaluation of 4-vinylcyclohexene. II. Induction of ovarian tumors in female B6C3F1 mice by chronic oral administration of 4-vinylcyclohexene [17].

References