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This consequently suppresses cadmium-induced changes in apoptosis-related proteins, inhibits cadmium-induced cell apoptosis, and prevents cadmium-induced mitochondrial transmembrane potential depolarization in PC12 cells [4]

The brain is especially vulnerable to oxidative damage, in part because of its high rate of oxidative activity and relatively low antioxidant capacity

doi: 10.1016/j.jtcme.2016.02.002

262 A parallel mechanism is observed in idiopathic pulmonary fibrosis (IPF), where telomere attrition in lung fibroblasts, combined with chronic inflammation and TGF- pathway activation, promotes excessive collagen deposition and irreversible structural damage