Journal
ENVIRONMENTAL TOXICOLOGY
Volume 31, Issue 10, Pages 1176-1184Publisher
WILEY
DOI: 10.1002/tox.22124
Keywords
cadmium; phospholipase A(2); proinflammation; mitochondrial dysfunction; phospholipid
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Funding
- Bharathidasan University (BDU), Tiruchirappalli, Tamilnadu, India
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Cadmium (Cd) is a toxic metal that is hazardous to health, and its exposure showed a significant reduction in mitochondrial phospholipid function in the rat testes. Cd induction enhanced phospholipases (PLA(2)s) activities, specifically the secretory PLA(2) and cytosolic PLA(2). There was a reduction in mitochondrial membrane potential and significant decline in the respiratory complexes, which was confirmed by 2D blue native gel. The mRNA expression of cyclooxygenase and proinflammatory cytokine genes interleukin (IL)-1, IL-6, tumor necrosis factor-, inducible nitric oxide synthase, and interferon- increased and that of anti-inflammatory cytokine IL-10 reduced with Cd exposure in a time-dependent manner. The gene expression of the proapoptotic factor Bax was elevated, and in parallel, the antiapoptotic factor Bcl2 was down-regulated. Hence, this study explored the testes under Cd toxicity and observed alterations in PLA(2)s and mitochondrial membrane composition/function and further explored the impact of these alterations on proinflammation and apoptosis. (c) 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1176-1184, 2016.
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