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The nephrotoxic effects of arsenic involve multiple interconnected mechanisms: Oxidative stress and kidney injury Arsenic metabolism generates ROS, initiating lipid peroxidation and compromising membrane integrity in renal tubular cells [32, 33]

Recently, several studies demonstrated that the NRF2-regulated antioxidant response is crucial for tissue homeostasis

T4 is converted to activated T3 in tissues located throughout the body

Notably, apoptosis is triggered in response to DNA damage resulting in nuclear p53 activation and consequent upregulation of pro-apoptotic proteins and their translocation to mitochondria to trigger the MOMP-mediated pathway

The decrease in absorbance at 412 nm serves as an indicator of GPX activity