Review Article
Glutathione “Redox Homeostasis” and Its Relation to Cardiovascular Disease
Table 1
Evidence from animal studies.
| Model | Species | Treatment | Effects | Ref |
| ApoE−/− | Mice | Liposomal coated GSH 50 mg/kg/day for 2 months | Reduction of AAPH oxidation and lipid peroxides and oxidation of LDL | [83] | ApoE−/− | Mice | OTC 500 mg/kg/day for 6 weeks | Increased level of GSH, reduction of cellular OS, and oxidation of LDL | [87] | ApoE−/− | Mice | | GSH is depleted in the atheroma-prone aortic arch | [86] | ApoE−/−/GCLM−/− | Mice | | Reduced level of GSH; atherogenesis | [90] | High saturated fat diet | Mice | N-Acetyl cysteine, oral for 4 weeks | Increased level of GSH; reduced cholesterol level in plasma and the liver | [84] | Transgenic human lipoprotein(a) | Mice | Ribose-cysteine 0.16 g/kg/day for 8 weeks | Increased level of GSH and GPx activity; antiatherogenic effect | [91] | Endothelial cells | Rat | Pretreatment with H2O2 24 h and Zn supplementation | Increased expression of GCS and synthesis of GSH | [106] | Macrophage cells | Murine | Homocysteine 50 μM | Reduced level of GSH; increased OS and GCS activity | [105] | Alloxan-induced hyperglycemia | Rabbit | | Different GSH redox cycles in different tissues (heart, brain, and liver) | [88] | Alloxan-induced hyperglycemia | Rabbit | Pioglitazone | Increased GSH system parameters | [89] |
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AAPH: 2,2-azobis(2-amidinopropane) dihydrochloride; ApoE−/−: apolipoprotein E-deficient mice; ApoE−/−/GCLM−/−: mice doubly deficient in apolipoprotein E and γ-glutamylcysteine synthetase; BSO: buthionine sulfoximine; DEM: diethyl maleate; GCS: γ-glutamyl cysteine synthetase; GSH: glutathione; GPx: glutathione peroxidase; H2O2: hydrogen peroxide; OS: oxidative stress; OTC: L-2-oxo-4-thiazolidin carboxylate (which supplies cysteine residues); Zn: zinc (in form ZnSO4).
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