Silymarin Attenuates Arsenic-Induced Mitochondrial Dysfunction and Suppression of Nrf2/ARE-Regulated Phase II...

Arsenic, an environmentally widespread and highly poisonous metalloid, presents major risks to health by interfering with cellular mechanisms and compromising mitochondrial performance. This research evaluated the mitigating effects of silymarin on arsenic-caused oxidative damage, reduced expression of phase II detoxification genes and mitochondrial impairments in rat brain cells. Adult Male Wistar rats received oral doses of arsenic (25 ppm) and/or silymarin (50 mg/kg body weight) for 28 days. Biochemical tests measured mitochondrial complex functions and molecular analyses assessed the expression of phase II antioxidant genes, mitochondrial formation indicators and associated regulatory elements. Arsenic treatment substantially inhibited Nrf2/ARE-controlled phase II detoxification genes and disrupted mitochondrial biogenesis processes. Conversely, silymarin administration notably recovered mitochondrial complex performance and enhanced the expression of genes linked to detoxification and biogenesis. These outcomes indicated that silymarin could act as an effective treatment option for reducing arsenic-related mitochondrial impairments.