Mechanisms underlying methamphetamine-induced disruption of testicular integrity

Methamphetamine (METH) abuse is a global health concern with serious repercussions, including potential disruption of the male reproductive system. Testicular integrity is particularly vulnerable to the toxic effects of METH. This review aims to comprehensively examine the current literature to elucidate the key mechanisms by which METH induces testicular damage, focusing on the cellular and molecular pathways involved. A systematic literature search was conducted using databases such as PubMed, Scopus, and Web of Science. Keywords included "methamphetamine," "testicular toxicity," "reproductive toxicity," "male infertility," "oxidative stress," "apoptosis," and "blood-testis barrier." Studies investigating the effects of METH on testicular function, morphology, and molecular markers were included. The review reveals that METH-induced testicular toxicity is mediated by multiple mechanisms, including increased oxidative stress, inflammation, disruption of the blood-testis barrier, apoptosis of germ cells and Sertoli cells, and alterations in hormone synthesis. Furthermore, METH can disrupt spermatogenesis and reduce sperm quality, potentially leading to infertility. METH significantly compromises testicular integrity through a complex interplay of oxidative stress, inflammation, blood-testis barrier disruption, and cellular apoptosis. Understanding these mechanisms is crucial for developing targeted interventions to mitigate the adverse reproductive effects of METH abuse and preserve male fertility.