N‐Acetylcysteine Protects From Glutathione Depletion in Rats Exposed to Hyperoxia

Abstract

NAC prevents oxidant stress during hyperoxic exposure, most likely by supplying cysteine as a precursor for GSH synthesis.

Different Mechanisms of c-Jun NH2-terminal Kinase-1 (JNK1) Activation by Ultraviolet-B Radiation and by Oxidative Stressors

“…This kinetics of activation resembled that observed in anisomycin-treated cells (Fig. 1, compare lanes 1-4 with lanes [25][26][27][28]. In contrast, the activity of JNK1 in cells treated with sodium arsenite was not substantially elevated 15 min after the treatment and displayed a slow, graded, increase during the 2 h postincubation period (Fig.…”

“…for the biosynthesis of GSH (27)(28)(29)(30). To investigate whether UV-B-induced activation of JNK is dependent on reactive oxygen intermediates, we employed pretreatment of Rat-1 cells with NAC (30 mM) for 30 min before challenging the cells with UV-B or other stimuli.…”

“…First, sodium arsenite, cadmium chloride, and H 2 O 2 activated JNK1 with relatively slow kinetics, whereas UV-B potentiated JNK1 activity rapidly. Second, pretreatment of cells with N-acetyl cysteine (NAC, a potent scavenger of H 2 O 2 , ⅐ OH, and HOCl (25,26) and a precursor for the biosynthesis of GSH (27)(28)(29)(30)) at physiological pH abolished the ability of all oxidative stressors tested to activate JNK1, but failed to affect the activation of JNK1 by UV-B or by another ribotoxic stressor, the antibiotic anisomycin. Third, emetine, an immediate inhibitor of ribosomal translocation and of UV-B-and anisomycin-induced activation of JNK1 (10,12), was unable to inhibit the activation of JNK1 by the oxidative stressors.…”

Nickel Mobilizes Intracellular Zinc to Induce Metallothionein in Human Airway Epithelial Cells

“…Thus, production of ROS may not be involved in Ni-induced MT2A, but free thiols may regulate the ability of Ni to induce certain genes. NAC acts as an antioxidant by increasing the intracellular free thiol pool and increasing synthesis of glutathione (GSH) (41). GSH and oxidized gluthothione (GSSG) are key regulators of the release of Zn from MT (42,43).…”

L-Cysteine Prevents Oxidation-Induced Block of the Cardiac Na+ Channel Via Interaction With Heart-Specific Cysteinyl Residues in the P-Loop Region.

“…N-acetyl-L-cysteine (NAC) has been clinically shown to prevent cardiac injuries induced by oxygen-derived free radicals 1 and it has been experimentally proven to protect the heart from ischemic insult by opening the ATP-sensitive K + channels (KATP). 2 Although the mechanisms by which L-cysteine exerts its protective effect are still unclear, it has been reported that L-cysteine or NAC enhances the cellular thiol pool to inactivate already formed radical species, [3][4][5][6] and that they could directly cancel oxidative stress by reducing sulfhydryl groups.…”