Since the rate of oxygen consumption is particularly high in brain tissues, production of reactive oxygen species (ROS) is accentuated in these vital cells, making them particularly vulnerable to oxidative damage and especially dependent upon the antioxidant protection provided by selenoenzymes. High mercury exposures deplete the amount of cellular selenium available for the biosynthesis of thioredoxin reductase and other selenoenzymes that prevent and reverse oxidative damage, which, if the depletion is severe and long lasting, results in brain cell dysfunctions that can ultimately cause death. Mercury in its various forms is particularly harmful to fetuses as an environmental toxin in pregnancy, as well as to infants. Women who have been exposed to mercury in substantial excess of dietary selenium intakes during pregnancy are at risk of giving birth to children with serious birth defects. Mercury exposures in excess of dietary selenium intakes in young children can have severe neurological consequences, preventing nerve sheaths from forming properly. Exposure to methylmercury causes increased levels of antibodies sent to myelin basic protein (MBP), which is involved in the myelination of neurons, and glial fibrillary acidic protein (GFAP), which is essential to many functions in the central nervous system (CNS). This causes an autoimmmune response against MBP and GFAP and results in the degradation of neural myelin and general decline in function of the CNS. Diagnosis
Diagnosis of elemental or inorganic mercury poisoning involves determining the history of exposure, physical findings, and an elevated body burden of mercury.
Vaginal adenosis is a benign  abnormality in the vagina, commonly thought to be caused by intrauterine and neonatal exposure of diethylstilbestrol and other progestogens and nonsteroidal estrogens, however it has also been observed in otherwise healthy women and has been considered at times idiopathic or congenital. Postpubertal lesions have also been observed to grow de novo. It has a rather common incidence, of about 10% of adult women. Causes
Vaginal adenosis is characterised by the presence of metaplastic cervical or endometrial epithelium within the vaginal wall, considered as derived from Müllerian epithelium islets in later life. In women who were exposed to certain chemicals, vaginal adenosis may arise in up to 90%. Since these contraceptives were discontinued, incidence has dropped dramatically. Risk is however still present in subsequent generations due to recent exposure.It is thought steroid hormones play a stimulatory growth in adenosis formation. Vaginal adenosis is also often observed in adenocarcinoma patients. Diagnosis
Colposcopically, it presents itself similarly to columnar epithelium on the cervix, assisted with lugols solution application for diagnosis. It can be discovered as nodules or cysts on the vaginal tube, with biopsy needed for further diagnosis. As seen cytologically, epithelial and stromal cells in vaginal adenosis show characteristic fusion through the basal lamina or with stromal fibroblasts. Adenosal cells can be distinguished as mucinous, tuboendometrial, and embryonic.