Rotenone induces nephrotoxicity in rats: oxidative damage and apoptosis

Toxicology Mechanisms and Methods
Xiao-Wen JiangWen-Hui Yu

Abstract

Previous studies have examined rotenone toxicity on the human central nervous system, especially in the pathogenesis of Parkinson's disease, but few have investigated the effects of rotenone on the kidney. Here, rotenone-induced nephrotoxicity was evaluated by determining morphological, biochemical, oxidative stress-related, and apoptotic factor alterations in rat renal tissue. Morphological and biochemical analyzes showed that rotenone administration to rats damaged renal tissue. Western blot results revealed that rotenone-induced oxidative damage, causing overproduction of glutathione, malonaldehyde, and reactive oxygen species (ROS), and inhibiting superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity. Rotenone also decreased the mitochondrial membrane potential and increased voltage-dependent anion channel (VDAC), caspase-3, and caspase-9 protein levels, indicating an association of apoptosis with renal damage. Our results suggest that glutathione, malonaldehyde, and ROS may be signals of rotenone-induced oxidative damage, and that the mitochondrial pathway plays a key role in apoptosis of renal cells following rotenone administration.

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Citations

Jun 4, 2019·Archives of Physiology and Biochemistry·Shambhoo Sharan TripathiSyed Ibrahim Rizvi
Jul 3, 2019·Daru : Journal of Faculty of Pharmacy, Tehran University of Medical Sciences·Whidul HasanDeepali Jat
Jul 10, 2020·Drug Metabolism Reviews·S Cyrus KhojastehDonglu Zhang
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Sep 26, 2019·Kidney & Blood Pressure Research·Wen ZhangSongming Huang

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Apoptosis

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