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Title:
l-Cysteine in vitro can restore cellular glutathione and inhibits the expression of cell adhesion molecules in G6PD-deficient monocytes | Amino Acids
Description:
l-Cysteine is a precursor of glutathione (GSH), a potent physiological antioxidant. Excess glucose-6-phosphate dehydrogenase (G6PD) deficiency in African Americans and low levels of l-cysteine diet in Hispanics can contributes to GSH deficiency and oxidative stress. Oxidative stress and monocyte adhesion was considered to be an initial event in the progression of vascular dysfunction and atherosclerosis. However, no previous study has investigated the contribution of GSH/G6PD deficiency to the expression of monocyte adhesion molecules. Using human U937 monocytes, this study examined the effect of GSH/G6PD deficiency and l-cysteine supplementation on monocyte adhesion molecules. G6PD/GSH deficiency induced by either siRNA or inhibitors (6AN/BSO, respectively) significantly (p < 0.005) increased the levels of cell adhesion molecules (ICAM-1, VCAM-1, SELL, ITGB1 and 2); NADPH oxidase (NOX), reactive oxygen species (ROS) and MCP-1 were upregulated, and decreases in levels of GSH, and nitric oxide were observed. The expression of ICAM-1 and VCAM-1 mRNA levels increased in high glucose, MCP-1 or TNF-α-treated G6PD-deficient compared to G6PD-normal cells. l-Cysteine treatment significantly (p < 0.005) increased G6PD activity and levels of GSH, and decreased NOX, ROS, and adhesion molecules. Thus, GSH/G6PD deficiency increases susceptibility to monocyte adhesion processes, whereas l-cysteine supplementation can restore cellular GSH/G6PD and attenuates NOX activity and expression of cell adhesion molecules.
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Keywords {🔍}

pubmed, article, google, scholar, cas, central, adhesion, cell, lcysteine, glutathione, deficiency, oxidative, stress, dehydrogenase, levels, jain, glucosephosphate, molecules, diabetes, gsh, human, med, glucose, endothelial, redox, blood, expression, monocyte, cardiovascular, type, clin, health, authors, function, content, data, african, vascular, supplementation, nox, mcp, high, cells, disease, protein, biol, mol, res, vitamin, privacy,

Topics {✒️}

tnf-α-treated g6pd-deficient compared n-acetyl-cysteine blunts 6-hydroxydopamine l-buthionine-sulfoximine-induced apoptosis glucose-6-phosphate dehydrogenase deficiency cysteine/cystine redox signaling excess glucose-6-phosphate dehydrogenase total anti-oxidant potential month download article/chapter sucrose-rich diet-induced hyperglycaemia l-cysteine treatment significantly glucose-6-phosphate dehydrogenase monocyte-endothelial cell interactions g6pd-deficient monocytes 3t3-l1 adipocytes exposed glutamate cysteine ligase rajesh parsanathan l-cysteine supplementation g6pd/gsh deficiency induced l-cysteine diet cell adhesion molecules l-cysteine efflux article parsanathan nadph oxidase isoforms elevated oxidative stress inhibits nf-kappab activation jain sk human u937 monocytes full article pdf research core facility l-cysteine metabolism nuclear factor-kappab streptozotocin-induced type increased g6pd activity monocyte adhesion molecules restore cellular gsh/g6pd deficient human fibroblasts cell adhesion modulated attenuates nox activity dose-response meta-analysis author information authors increases blood levels privacy choices/manage cookies cell mol immunol american heart association related subjects impaired immune responses mexican adult population enhanced oxidative stress l-cysteine monocyte adhesion processes

Questions {❓}

Jain SK, Kahlon G, Bass P, Levine SN, Warden C (2015) Can l-cysteine and vitamin D rescue vitamin D and vitamin D binding protein levels in blood plasma of African American type 2 diabetic patients?
Jain SK, Manna P, Micinski D, Lieblong BJ, Kahlon G, Morehead L, Hoeldtke R, Bass PF 3rd, Levine SN (2013) In African American type 2 diabetic patients, is vitamin D deficiency associated with lower blood levels of hydrogen sulfide and cyclic adenosine monophosphate, and elevated oxidative stress?
Yoshimura T (2018) The chemokine MCP-1 (CCL2) in the host interaction with cancer: a foe or ally?

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