Total Antioxidant Capacity of Saliva in Children with HIV

Several recent reports have indicated high levels of reactive oxygen species, causing oxidative stress, in the pathogenesis of HIV infection. Oxidative stress may lead to enhanced HIV replication in infected cells and may also aggravate the immunodeficiency by reduction of cellular immunity and possibly by increased programmed cell death of lymphocytes. Saliva can constitute a first line of defense against free radical mediated oxidative stress. The use of saliva as a diagnostic fluid has become somewhat of a translational research success story. Technologies are now available enabling saliva to be used to diagnose disease and predict disease progression.

Purpose: The antioxidant capacity of saliva was investigated in 68 children who were divided into two groups. 34 children who were investigated were diagnosed as having HIV infection and the other group consisted of children who reported to the department and served as healthy controls. Total antioxidant capacity of saliva was evaluated by spectrophotometric assay.

Conclusions: The results indicated that the total antioxidant capacity (TAC) of saliva decreased in children with HIV infection. TAC was seen to increase with the age of the children.

HIV; Oxidative stress; total antioxidant capacity (TAC)

1. Halliwell B.Antioxidants: the basics-what they are and how to evaluate them. In: Antioxidants in disease mechanisms and therapy. Advances in pharmacology. San Diego: Academic Press, 1997, 38: 3–20.

2. Sies H, Tsunemitsu A, Matsumura T. Antioxidants in disease mecha-nisms and therapy. Stomatologiia, 73(1): 11–13. 1997.

3. Devasagayam TP, Tilak JC, Boloor KK, Sane KS. Free radicals and antioxidants in human health: current status and future prospects. J Assoc Physicians India, Oct; 52: 794–804, 2004.

4. Yamazaki I, Piette LH. ESR Spin Trapping studies on the reaction of Fe++ions with H2O2 reactive species in O2 toxicity in biology. J Biol Chem; 265:189-94. 1990.

5. Amitha M Hegde, Kavita Rai, Vivek P. Total Antioxidant Capacity of Saliva and Its Relationship with ECC and Rampant Caries. J Clin Pedi-atr Dent, 33(3): 231–234, 2009.

6. Sreebny LM et al. Saliva: It’s Role in Health and Disease. International Dental Journal, 42: 291–304, 1992.

7. Prieto, Pineda M, Aguilar M. Spectrophotometric Quantitation of Antioxidant Capacity through the formation of a Phosphomolybdenum Complex: specific application to the determination of Vit E. Analytical Biochemistry, 269: 337–341, 1999.

8. Strekfus CF, Bigler LR. Saliva as a diagnostic fluid. Oral Diseases, 8: 69–76, 2002.

9. John T. McDevitt. Saliva as the next best diagnostic tool. Journal of Biochem, 45(2): 23–25, 2006.

10. Pereslegina IA. The activity of antioxidant enzymes in the saliva of nor-mal children. Laboratornoe Delo, 11: 20–23, 1989.

11. Prior R.L, Cao G. In vivo total antioxidant capacity: comparison of dif-ferent analytical methods. Free Radical Biology & Medicine, 27: 1173–1181, 1999.

12. Thomas JA. Oxidative stress, oxidant defense, and dietary constituents. In: Shils ME, Olson JA, Shike M, eds. Modern nutrition in health and disease. Eighth ed. Philadelphia: Lea & Febiger, 1994, p. 501–512.

13. Greenspan HC and Aruoma OI. Oxidative stress and apoptosis in HIV infection: a role for plant-derived metabolites with synergistic antioxi-dant activity. Immunology Today, 15: 209–213, 1994.

14. Dworkin BM, Wormser GP, Axelrod F, et al. Dietary intake in patients with AIDS, patients with AIDS-related complex and sero-logically pos-itive HIV patients: correlations with nutritional status. JPEN J Parenter Enteral Nutr, 14: 605–9, 1990.

15. Kapembwa M, Bridges C, Joseph AE, Fleming SC, Batman P, Grif-fin GE. Ileal and jejunal absorptive function in patients with AIDS and enterococcidial infection. J Infect; 21: 43–53, 1990.

16. Mondal D, Pradhan L, Ali M, Agrawal KC. HAART drugs induce oxidative stress in human endothelial cells and increase endothelial recruitment of mononuclear cells: exacerbation by inflammatory cytokines and amelioration by antioxidants. Cardiovascular Toxicol, 4(3): 287–302, 2004.