{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,11]],"date-time":"2026-09-11T03:34:15Z","timestamp":1789097655078,"version":"build-2803163510"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,8,4]],"date-time":"2025-08-04T00:00:00Z","timestamp":1754265600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Environmental Toxicology"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Cadmium (Cd), a heavy metal, disrupts the structure of seminiferous tubules and induces cell death at multiple stages of sperm development. Cd also impairs Leydig cells (LCs), resulting in reduced serum testosterone (T) levels. This study primarily examined the impact of Cd on the mitochondrial compartment and mitochondrial\u2010associated endoplasmic reticulum membranes (MAMs) in rat testis. Additionally, the potential of D\u2010aspartate (D\u2010Asp) to mitigate Cd\u2010induced effects on steroidogenesis and spermatogenesis was assessed by administering D\u2010Asp simultaneously or preventively with Cd. The findings demonstrated that Cd exerts reprotoxicity by affecting the mitochondrial compartment and MAMs, evidenced by an imbalance in mitochondrial dynamics, impaired mitophagy pathway, and downregulated mitochondrial biogenesis. Cd exposure also reduced lipid transfer\u2010related factor expression and increased ER stress. Moreover, elevated levels of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    transfer\u2010related proteins, indicative of perturbed Ca\n                    <jats:sup>2+<\/jats:sup>\n                    homeostasis, may be associated with enhanced oxidative stress and apoptosis, which are known effects of Cd. Immunofluorescent analysis revealed that the Cd\u2010induced mitochondrial and MAMs damage was prominent in LCs, spermatocytes, and spermatids, confirming the metal's adverse effects on steroidogenesis and spermatogenesis. Conversely, co\u2010administration or preventive administration of D\u2010Asp with Cd preserved mitochondrial homeostasis and functional ER\u2010mitochondria interactions. In conclusion, the study offers novel insights into the cellular mechanisms underlying Cd\u2010induced reprotoxicity. Importantly, it highlights the efficacy of D\u2010Asp in preventing or counteracting testicular damage caused by Cd by enhancing mitochondrial and MAMs functionality.\n                  <\/jats:p>","DOI":"10.1002\/tox.24559","type":"journal-article","created":{"date-parts":[[2025,8,4]],"date-time":"2025-08-04T13:00:56Z","timestamp":1754312456000},"page":"18-32","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Cadmium\u2010Induced Mitochondrial and\n                    <scp>MAMs<\/scp>\n                    Dysregulation in Rat Testis: The Protective Role of D\u2010Aspartate"],"prefix":"10.1002","volume":"41","author":[{"given":"Debora","family":"Latino","sequence":"first","affiliation":[{"name":"Department of Environmental, Biological and Pharmaceutical Sciences and Technologies University of Campania \u201cLuigi Vanvitelli\u201d  Caserta 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