There has been little work in vivo investigating the effects of pesticides on Bcl-2 family members and none, to our knowledge, investigating the effects of MXC on Bcl-2 family members in the ovary. Still, some studies have looked at other chemicals, and previous studies conducted in Bax-deficient mouse models found some protection from toxicant-induced apoptosis in primordial follicles and oocytes. For example, Takai et al. found that Bax-deficient mice were partially protected by the effects of the industrial chemical and primordial follicle toxicant, 4-vinylcyclo-hexene diepoxide.
Bax-deficient mice were also protected from destruction of oocytes by the chemotherapeutic agent doxorubicin. Previous studies also have utilized transgenic mouse models that overexpress Bcl-2 to test whether Bcl-2 overexpression protects against toxicant-induced apoptosis, although none have looked at MXC. For instance, the EW36 cell line, a human cell line that overexpresses Bcl-2, was found to be more resistant to apoptosis induced by a variety of toxicants. Morita et al. found that oocytes obtained from transgenic mice expressing higher amounts of Bcl-2 (with overexpression being driven by the zona pellucida 3 gene promoter) were more resistant to chemotherapy-induced apoptosis.