Erythrocyte nitric oxide synthase as a surrogate marker for mercury-induced vascular damage: The modulatory effects of naringin

Authors

  • Gamaleldin I. Harisa,

    1. Department of Pharmaceutics, Kayyali Chair for Pharmaceutical Industry, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
    2. Department of Biochemistry, College of Pharmacy, Al-Azhar University (Boys), Cairo, Egypt
    Search for more papers by this author
  • Amr D. Mariee,

    Corresponding author
    1. Department of Biochemistry, College of Pharmacy, Al-Azhar University (Boys), Cairo, Egypt
    2. Department of Pharmacology and Toxicology, College of Pharmacy, Taibah University, Al-Madinah Al-Munawwarrah, Saudi Arabia
    Search for more papers by this author
  • Osama M. Abo-Salem,

    1. Department of Pharmacology and Toxicology, College of Pharmacy, Al-Azhar University (Boys), Cairo, Egypt
    2. Department of Medical Laboratories, College of Applied Medical Sciences, Taif University, Taif, Saudi Arabia
    Search for more papers by this author
  • Sabry M. Attiaa

    1. Department of Pharmacology and Toxicology, College of Pharmacy, Al-Azhar University (Boys), Cairo, Egypt
    2. Department of Pharmacology and Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Saudi Arabia
    Search for more papers by this author

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), math formula- 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. © 2013 Wiley Periodicals, Inc. Environ Toxicol 29: 1314–1322, 2014.

Ancillary