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Glutathione peroxidase (EC 1.11.1.9) and superoxide dismutase (EC 1.15.1.1) activities in riboflavin-deficient rats infected with Plasmodium berghei malaria

Published online by Cambridge University Press:  09 March 2007

D. A. Adelekan  and
D. I. Thurnham
D. A. Adelekan*
Affiliation:
Department of Community Health, Faculty of Clinical Sciences, College of Health Sciences, Obafemi Awolowo University, Ile-lfe, Nigeria
D. I. Thurnham
Affiliation:
Northern Ireland Centre for Diet and Health, School of Biomedical Sciences, University of Ulster, Coleraine BT52 1SA, UK
*
*Corresponding author:Dr D. A. Adelekan, email adel@chs.oauife.edu.ng and dadeleka@oauife.edu.ng
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Abstract

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Riboflavin deficiency interferes with the growth and multiplication of malaria parasites as well as the host response to malaria. The objective of the present work was to determine the effects of riboflavin deficiency on erythrocyte glutathione peroxidase (EC 1.11.1.9; GPx) and superoxide dismutase (EC 1.15.1.1; SOD) in rats infected with Plasmodium berghei malaria. Riboflavin in its co-enzyme form, FAD, is required by glutathione reductase (EC 1.6.4.1) to regenerate GSH and GSH is an important cellular antioxidant both in its own right and also as a substrate for the enzyme GPx. Weanling rats were deprived of riboflavin for 8 weeks before intraperitoneal injection of 1 × 106P. berghei parasites. Control animals were weight-matched to the respective riboflavin-deficient group. At 10d post-infection, parasite counts were higher in the weight-matched control group than the riboflavin-deficient group (P = 0.004). GPx activity was higher in erythrocytes of rats parasitized with P. berghei than comparable non-infected rats regardless of riboflavin status (P < 0.05). As mature erythrocytes do not synthesize new protein, the higher GPx activities were probably due to the presence of the parasite protein. In erythrocytes from riboflavin-deficient rats, GPx activity tended to be lower than in those rats fed on diets adequate in riboflavin (weight-matched controls) whether parasitized or not, but the difference was not significant. Neither riboflavin deficiency nor malaria had any effect on erythrocyte SOD activity. It was concluded that riboflavin deficiency has no marked effect on erythrocyte GPx or SOD activity in the rat.

Keywords

RiboflavinMalariaGlutathione peroxidaseSuperoxide dismutase
Type
Research Article
Information
British Journal of Nutrition , Volume 79 , Issue 3 , March 1998 , pp. 305 - 309
Copyright
Copyright © The Nutrition Society 1998

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