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Excessive ROS triggers oxidative stress Although ROS production in mitochondria is in balance with an intracellular antioxidant system under physiological conditions, the balance is easy to be disrupted under pathological conditions, such as radiation, hypoxia, cytokines, hyperlipidemia, and hyperglycemia, which results in the accumulation of ROS, facilitating oxidative stress, cell damage, and diseases, such as cancer, cardiovascular disease, neurological disease, respiratory disease, and so on

Comparison between mean levels (SD) of superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT) enzymes in the studied group and control children

Its primary metabolic effects result from the activation of SIRT1 and AMPK (20), which in turn enhance mitochondrial biogenesis, improve insulin sensitivity through LKB1 activation (21, 22), and decrease de novo lipogenesis by ACC phosphorylation and SREBP-1c/ChREBP downregulation (23)

Or Are Both Caused by Insulin Resistance

Catalase overexpression impairs TNF-alpha induced NF-kappaB activation and sensitizes MCF-7 cells against TNF-alpha

doi: 10.1016/j.mehy.2020.109862 220 PoljsakB.uputD.MilisavI