Short communicationEffect of cisplatin on the activities of enzymes which protect against lipid peroxidation
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Cited by (129)
Repurposing FDA-approved drugs against the toxicity of platinum-based anticancer drugs
2022, Life SciencesCitation Excerpt :Increased PKG activity also prevents the mitochondrial membrane potential loss induced by cisplatin in the tubular cells (Table 1) [83]. Toxic, highly reactive oxygen free radicals are induced by cisplatin, which causes a rise in lipid peroxidation and a decrease in the enzyme activity that protects the body from lipid peroxidation as well as a reduction in the body's antioxidant status and results in nephrotoxicity [84–86]. Furthermore, reactive nitrogen species have been linked to the mechanism of nephrotoxicity induced by cisplatin, which is characterized by a rise in renal peroxynitrite and nitric oxide levels [87,88].
Protective effects of sesamol against cisplatin-induced nephrotoxicity in rats: A mechanistic approach
2020, Obesity MedicineCitation Excerpt :Nephrotoxicity is one of the major toxic side effect in 20% of cisplatin-treated cancer patients, which limiting its use in chemotherapy (Dos et al., 2012). Oxidative stress induced by CP treatment in cancer patients, activates various inflammatory mediators that promote lipid oxidation and causes DNA damage in proximal and distal tubules in the kidney (Sadzuka et al., 1992). Antioxidants showed various pharmacological activities and spread widely in nature.
Persistent increase in mitochondrial superoxide mediates cisplatin-induced chronic kidney disease
2019, Redox BiologyCitation Excerpt :It is known that the major site of cisplatin-induced nephrotoxicity is in proximal tubule cells [3], where cisplatin forms glutathione (GSH) and cysteine conjugates, which undergo metabolic activation to form reactive thiols [18]. Cisplatin accumulates in the mitochondria of tubular epithelial cells, causes mitochondrial structural damage, increases in steady-state levels of reactive oxygen species (ROS), and decreases in total GSH and superoxide dismutase (SOD) activity [16,19–21]. Impaired mitochondrial metabolism reduces mitochondrial electron transport chain (ETC) efficiency, increases ROS—more specifically superoxide (O2•-)—and reduces ATP generation [13,15,21,22].
Insights into the protective capacity of human dental pulp stem cells and its secretome in cisplatin-induced nephrotoxicity: effects on oxidative stress and histological changes
2023, Journal of Basic and Clinical Physiology and PharmacologyLipid peroxidation of immune cells in cancer
2023, Frontiers in Immunology