Role of oxidative stress in single‐dose, cadmium‐induced testicular cancer

Abstract

Treatment of rats with a single carcinogenic dose of CdCI₂ (i.e., 30 nmol/kg) caused severe hemorrhagic damage in the testis within the first 12 h after the metal. Subsequently, atrophy with calcification developed in the next 2–3 mo. Atrophied tissues regenerated during the 1 yr after exposure. Twelve hours after exposure to the Cd treatment, lipid peroxidation levels, Fe content, and cellular production of H₂O₂ were remarkably elevated in testicular Leydig cells, the target cell population for Cd carcin‐ogenesis. At the same time, glutathione peroxidase activity rose, glutathione reduc‐tase and catalase activities were reduced, and superoxide dismutase activity was unchanged. Xanthine oxidase activity in Leydig cells was also elevated at 6 and 9 h after the Cd treatment. Reduced glutathione in testes was decreased and oxidized glutathione was increased 12 h after exposure to the metal. These facts suggest that the carcinogenic doses of Cd induced oxidative stress while compromising cellular defense mechanisms against such stress. Therefore, active oxygen species such as H₂O₂ may have an important role in the initiation of carcinogenesis within the target cell population.