mitochondrial damage glutathione in Cellular Redox Homeostasis and Disease Manifestation Mitochondrial reactive oxygen species cause

Association of arsenic levels in soil and water with urinary arsenic concentration of residents in the vicinity of closed metal mines

Differential enhancement of -glutamyl transpeptidase and -glutamylcysteine synthetase by tert-butylhydroquinone in rat lung epithelial L2 cells

Although dietary lipids encompass triacylglycerols, phospholipids, sterols (predominantly cholesterol with minor phytosterols), and small amounts of free fatty acids 10,11 only fatty acyl chains are oxidizable for yielding energy, whereas cholesterol is catabolized chiefly to bile acids rather than used as an energy substrate 12

Nevertheless, the availability of in situ techniques is undoubtably an important development that is adding to the repertoire of tools to analyze the complexities of glutathione homeostasis and related issues of cellular redox metabolism

Gln depletion therapy can inhibit Gln metabolism in tumor cells, but in colon cancer, it has been observed that Gln depletion promotes the expression of the aspartate/glutamate transporter SLC1A3 in tumor cells, increasing the intracellular glutamate concentration and promotes Gln synthesis

Glutathione: antioxidant properties dedicated to nanotechnologies Antioxidants (Basel)