Low‐dose heavy metal mixture (lead, cadmium and mercury)‐induced testicular injury and protective effect of zinc andCostus aferin wistar albino rats

Abstract

Global concern about male infertility is growing, and this affects approximately 50% of infertile couples (Agarwal, Mulgund, Hamada, & Chyatte, 2015). Environmental and occupational exposures to heavy metals have led to various deleterious damages to the biological system, of which infertility is one. The results of various studies associate male factors with infertility in 20%-50% of cases (Boivin, Bunting, Collins, & Nygren, 2007; Jarow et al., 2002). Aetiological factors implicated in male infertility can be categorised as follows: (a) pre-testicular, such as endocrine and coital disorders; (b) testicular, including abnormalities of sperm production; and (c) post-testicular, such as anatomic obstructions (Carvalho, Zhang, & Lupski, 2011). Various environmental toxicants such as lead (Pb), cadmium (Cd) and mercury (Hg) have been reported to adversely affect spermatogenesis in man and rats, which can cause low sperm count, abnormal sperm morphology and poor semen quality (Agarwal et al., 2015; Wong. et al., 2010), released by the industrial processes and natural forces into our surroundings. As a result, humans are exposed by inhalation of polluted air, consumption of contaminated food and water and usage

Etlingera hemisphaerica Blume attenuates male reproductive toxicity due to mercury chloride in Mus musculus

“…The antioxidant indicators (catalase, CAT; superoxide dismutase, SOD; and GSH) were reduced, and the lipid peroxidation marker was raised by a low-dose heavy metal combination (LDHMM; PbCl 2 +CdCl 2 +HgCl 2 ). Costus afer treatment decreased LDHMM-mediated toxicity in rats in a dose-dependent manner [49]. The results of this study indicate that treatment with HgCl 2 (5 mg/kg bw) on d-1 signi cantly increased MDA levels compared to the control on d-7.…”

Effects of naringenin on oxidative damage and apoptosis in liver and kidney in rats subjected to chronic mercury chloride

“…30 In various studies, it was reported that radical production increases as a result of mercury chloride exposure, leading to lipid peroxidation in the cell and causing damage in many tissues, especially in the kidney and liver. 2,30,31 In this study, it was found that liver and kidney MDA levels were significantly increased as a result of mercury chloride exposure (Tables 1 and 2). The increase in liver and kidney MDA levels is a clear indication that mercury chloride exposure causes oxidative damage.…”

“…Although MDA is the end product formed after the peroxidation of unsaturated fatty acids, it is an important lipid peroxidation marker to show the level of damage indirectly, although not directly 30 . In various studies, it was reported that radical production increases as a result of mercury chloride exposure, leading to lipid peroxidation in the cell and causing damage in many tissues, especially in the kidney and liver 2,30,31 . In this study, it was found that liver and kidney MDA levels were significantly increased as a result of mercury chloride exposure (Tables 1 and 2).…”