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Jonathan L. Tilly and James K. Pru Background: Exposure to certain industrial chemicals has been shown to cause premature death of the stockpile of female germ cells mammals are born with. If this effect occurs in women as well, it could cause premature menopause leading to other hormonally related conditions. This was the focus of a previous report by these investigators (Nat Genet. 2001 Aug;28(4):355-60). In the earlier report compounds known as polycyclic aromatic hydrocarbons (PAHs), but not dioxin, were shown to signal through the Ah receptor/Bax-regulated pathway leading to oocyte death. Advance: In a new report the investigators have expanded their work to include the environmental agent 4-vinylcyclohexene diepoxide (VCD). VCD is a by-product of the manufacture of plastics, rubber, flame retardants, and pesticides. VCD has also been shown to also cause premature death of immature follicles from the ovaries of rats and mice. The current study shows that mice lacking the Bax gene retained more of their follicles than wild-type females when exposed to VCD. The same was true for mice lacking genes for the enzymes caspase-2 and caspase-3; enzymes essential in the life cycle of follicles. Implication: These results add to the tremendous progress that has been recently made in understanding the cellular and molecular events responsible for oocyte death and follicle depletion under normal and pathological conditions. Future research aimed at finding natural substances that will modify or incapacitate these proteins may lead to methods to prevent oocyte loss in response to the natural aging process and from exposure to environmental agents. Citation: Takai Y, Canning J, Perez GI, Pru JK, Schlezinger JJ, Sherr DH, Kolesnick, RN, Yuan J, Flavell RA, Korsmeyer SJ, Tilly JL. Bax, caspase-2, and caspase-3 are required for ovarian follicle loss caused by 4-vinylcyclohexene diepoxide exposure of female mice in vivo. Endocrinology. 2003 Jan;144(1):69-74. |
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