Figure 3

An update in the utilization of N-acetyl cysteine & vitamin c for tackling the oxidative stress in acute kidney injury secondary to robust sepsis - A systematic review

Kulvinder Kochar Kaur*, Gautam Allahbadia and Mandeep Singh

Published: 01 February, 2022 | Volume 6 - Issue 1 | Pages: 001-018

jcn-aid1084-g003

Figure 3:

Courtesy ref no-15-Adaptive and maladaptive reactions of the mitochondria to sepsis- stimulated induced oxidative stress. Escalated generation of superoxide (O2−) by nicotinamide adenine dinucleotide phosphate (NADPH) oxidase coupled with the reduction in action of manganese superoxide dismutase (MnSOD) causes accrual of O2−. Cytosolic nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) reacts with O2−, forming the highly reactive peroxynitrite (ONOO−). The accrual of O2− and ONOO− causing continued oxidative stress along with adecrease in mitochondrial membrane potential (ψm) and so mitochondrial impairment. In the case of localized mitochondrial injury, mitochondrial quality control modes are activated which arrest mitochondrial impairment. In addition to restrict escalated mitochondrial depletion. Recruitment of mitochondrial fission proteins to sites of damage targets the injured regions of the mitochondrion for fission. Subsequently, ubiquitin, PTEN-induced kinase (PINK1) and E3 ubiquitin-protein ligase (Parkin) proteins areenrolled to the injured mitochondrion, removed by mitochondrial fission and crosstalk with phagophore, consequently generating an autophagosome. The healthy regions of the mitochondrion undergoes mitochondrial fusion, that adds to the existing mitochondrial pool and restricting escalated mitochondrial depletion. Conversely, Comprehensive injury to mitochondria in robust, sepsis causes the liberation of cytochrome c oxidase, along with in the f generation of an apoptosome when it crosstalks with apoptotic protease activating factor-1 (Apaf-1) monomers as well as pro-caspase 9. This results in downstream activation of caspase 3/7, ultimately causing the containment of sepsis-induced injury via apoptosis. Mitochondrial dynamin-like GTPase (OPA-1); dynamin related protein-1 (DRP-1); damage-associated molecular patterns (DAMPs).

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