Preventive Effect of Zinc Against Cadmium-induced Oxidative Stress in the Rat Testis

Abstract

Abstract. The aim of this study was to investigate the antioxidant role of zinc (Zn) in the Cd-exposed testes of Wistar rats. Subchronic exposure to Cd (CdCl2, 40 mg/l, per os) for 30 days resulted in a significant reduction in growth rate (-11%) and relative weights of testes (-36%) and seminal vesicles (-80%). Treated rats displayed a decrease in testicular and plasma testosterone levels, respectively (-70%, P<0.05; -48%, P<0.05), epididymal sperm count (-22%, P<0.05), and spermatozoa motility (-35%, P<0.05). In contrast, Cd increased the malondialdehyde (+46%, P<0.05), metallothionein (+200%, P<0.05), and 8-oxodGuo concentrations (+71%, P<0.05) in the testis. In the gonad, Cd decreased the GPx (-30%, P<0.05), CAT (-32%, P<0.05), mitochondrial Mn-SOD (-34%, P<0.05), and cytosolic CuZn-SOD (-32%, P<0.05) activities. Zinc supplementation (ZnCl2, 40 mg/l, per os) in the Cd-exposed rats restored the activities of GPx, CuZn-SOD, and Mn-SOD in the testes to the levels of the control group. Moreover, zinc administration was capable of reducing the elevated levels of malondialdehyde in the testis. Interestingly, zinc supplementation attenuated DNA oxidation induced by Cd in the gonad and restored the testosterone level and sperm count to the levels of the control group. Zinc administration minimized oxidative damage and reversed the impairment of spermatogenesis and testosterone production induced by Cd in the rat testis.

Cadmium Toxicity Revisited: Focus on Oxidative Stress Induction and Interactions with Zinc and Magnesium

“…It seems that ROS production has an important role in chronic Cd nephrotoxicity (45), immunotoxicity (46), and carcinogenesis (47). On the other hand, chronic exposure to Cd often elevates tissue GSH, without elevating tissue LPO levels (37,45). This is confi rmed by our own results (38), which showed initial increase in liver LPO and Fe levels 24 h after a single oral dose, which dropped after repeated Cd dosing.…”

“…The author described Cd-induced production of reactive oxygen species (ROS) through interaction with critical subcellular sites such as mitochondria, peroxisomes, and microsomes, that resulted in the generation of free radicals and LPO in subcellular membranous structures. Production of ROS has been reported later in a variety of cell culture systems, as well as in intact animals via all routes of exposure (34)(35)(36)(37). We also found early signs of oxidative stress in the liver of mice exposed to a single oral Cd dose (20 mg kg -1 b. w. in the form of CdCl 2 ) through increased LPO level, expressed as malondialdehyde (MDA) after 6 h, 12 h, and 24 h (38).…”

Effect of combinations of four trace elements on cadmium bioaccumulation in a few tissues of male albino rats

“…Thus toxicity of Cd may result from disturbances in Zn metabolism, leading to the description of Cd as an antimetabolite of Zn. The most compelling reason for the protective effects of Zn against Cd toxicity is that Zn induces the protection of the metal binding protein metallothionein (MT) (Salem et al, 2008, Bonda et al, 2004. Hence, this may be the cause for lowering the concentration of Cd in the select tissues primarily in 30d kidney (8.327±0.450 µg/g).…”

Comparison of Antioxidant Effects of Kolaviron and Vitamin C Interventions on Testicular Structures Following Nevirapine Administration in Sprague-Dawley Rats

“…Testicular structures of HAART treated animals were noted with necrotic germ cells and a decrease of almost all morphometric and stereological testicular parameters (Azu et al). Necrosis and apoptotic death was one of the mechanisms responsible for the massive elimination of germ cells due to testicular toxicity (Amara et al, 2008;Li et al, 2010).…”