title: Erythrocyte nitric oxide synthase as a surrogate marker for mercury-induced vascular damage: the modulatory effects of naringin.
abstract: In this study, endothelial nitric oxide synthase activity and nitric oxide (NO) production by human erythrocytes in the presence and absence of mercuric chloride (HgCl2 ), L-arginine (L-ARG), N ω- nitro-L-arginine methyl ester (L-NAME), and naringin (NAR) were investigated. In addition, the levels of reduced glutathione (GSH) and related enzymes were estimated in erythrocytes hemolysate. The protein carbonyl content (PCC) and thiobarbituric acid-reactive substances (TBARS) levels were also determined. The results of this study revealed that the treatment of erythrocytes with either HgCl2 or L-NAME induced a significant decrease in NOS activity and nitrite levels compared with control cells. Furthermore, mercury exposure significantly increased the levels of PCC and TBARS but reduced the GSH level. The activities of glucose-6-phosphate dehydrogenase, glutathione reductase, glutathione peroxidase, and glutathione-S-transferase (GST) were inhibited. The exposure of erythrocytes to HgCl2 in combination with L-ARG, NAR, or both ameliorated the investigated parameters compared with erythrocytes incubated with HgCl2 alone. These results indicate that mercury exposure decreased both erythrocyte NOS activity and nitrite production, and that these parameters might be indicative of mercury exposure. The data also suggest that concomitant treatment with NAR can restore NO bioavailability through either its metal-chelating properties or its antioxidant activity.
authors: Department of Pharmaceutics, Kayyali Chair for Pharmaceutical Industry, College of Pharmacy, King Saud University, P.O. Box 2457, Riyadh 11451, Saudi Arabia; Department of Biochemistry, College of Pharmacy, Al-Azhar University (Boys), Cairo, Egypt.
authors: Gamaleldin I
authors: GI
authors: Harisa
authors: Amr D
authors: AD
authors: Mariee
authors: Osama M
authors: OM
authors: Abo-Salem
authors: Sabry M
authors: SM
authors: Attiaa
mesh_terms: D000975:Antioxidants / Q000494:pharmacology*; D001120:Arginine / Q000494:pharmacology; D015415:Biomarkers / Q000378:metabolism; D004785:Environmental Pollutants / Q000633:toxicity*; D004912:Erythrocytes / Q000187:drug effects* / Q000378:metabolism; D044950:Flavanones / Q000494:pharmacology*; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006461:Hemolysis; D006801:Humans; D015227:Lipid Peroxidation / Q000187:drug effects; D008627:Mercuric Chloride / Q000633:toxicity*; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D009573:Nitrites / Q000378:metabolism; D010084:Oxidation-Reduction; D050050:Protein Carbonylation; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D004785:Environmental Pollutants; D044950:Flavanones; D009573:Nitrites; D017392:Thiobarbituric Acid Reactive Substances; D009569:Nitric Oxide; D008627:Mercuric Chloride; D001120:Arginine; D005954:Glucosephosphate Dehydrogenase; D005979:Glutathione Peroxidase; D019001:Nitric Oxide Synthase; D005980:Glutathione Reductase; D005978:Glutathione; C005274:naringin; D019331:NG-Nitroarginine Methyl Ester
keywords: erythrocyte; mercury; naringin; nitric oxide; oxidative stress