Leydig Cell Toxicology

Several agents have been identified as Leydig cell toxicants, including ethanol, ethane 1,2 dimethanesulphonate (EDS), 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCCD), and steroid hormone receptor antagonists. These toxicants can damage Leydig cells in three ways: overstimulation or inhibition of steroidogenesis, induction of tumor formation, and promotion of cell death. Leydig cells are vulnerable to several toxins through direct actions and/or by disruption of the hypothalamic-pituitary axis.

Toxicants, such as ethanol, interfere with Leydig cell steroidogenesis by interfering with LH secretion, LH receptor binding, intracellular signal transduction pathways, and steroidogenic enzyme activities. Ethanol, for example, decreases LH secretion and reduces LH receptor binding and intracellular cyclic guanosine 5'-monophosphate (GMP) levels. Hence, chronic alcohol abuse causes declines in testosterone levels (138-140). Tumor formation and cell death are also observed after toxicant exposures. Carcinogenesis is considered to be a consequence of multiple insults to the genome. Necrosis and apoptosis have both been implicated in the process of toxicant-related Leydig cell death, with ethylene dimethanesulfonate exposure as the experimental paradigm (141).

Beat The Battle With The Bottle

Beat The Battle With The Bottle

Alcoholism is something that can't be formed in easy terms. Alcoholism as a whole refers to the circumstance whereby there's an obsession in man to keep ingesting beverages with alcohol content which is injurious to health. The circumstance of alcoholism doesn't let the person addicted have any command over ingestion despite being cognizant of the damaging consequences ensuing from it.

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