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Elevated glutathione S-transferase activity in erythrocytes from malnourished children
1Tropical Metabolism Research Unit, University of the West Indies, Kingston, Jamaica.
Insights
Severe malnutrition in children significantly increases erythrocyte glutathione S-transferases (GSTs), enzymes crucial for detoxification. This suggests oxidative stress plays a key role in the development of malnutrition.
Area of Science:
- Biochemistry
- Pediatrics
- Nutritional Science
Background:
- Glutathione S-transferases (GSTs) are vital detoxification enzymes.
- GSTs can be induced by increased substrate flux, such as during oxidative stress or antioxidant deficiency.
Purpose of the Study:
- To investigate if severe malnutrition induces GSTs in erythrocytes.
- To test the hypothesis that oxidative stress in malnutrition leads to GST induction.
Main Methods:
- Erythrocyte GST activity was measured using 1-chloro-2,4-dinitrobenzene (CDNB) as a substrate.
- The study included 271 malnourished children across four categories and 48 healthy children.
Main Results:
- Malnourished children exhibited significantly higher GST activity compared to healthy controls (P < 0.01).
- GST activity did not differ among the four malnutrition classifications.
- Higher GST activity was observed in children who died compared to survivors; no change was noted with anthropometric recovery.
Conclusions:
- Erythrocyte GST is induced in children suffering from severe malnutrition.
- This induction likely results from prolonged oxidative stress exposure preceding the clinical presentation of malnutrition.
Abstract:
Glutathione S-transferases (GSTs) are principally involved in detoxification. These enzymes can be induced by an increased flux of substrate, such as occurs during pro-oxidative stress or antioxidant deficiency. We tested the hypothesis that the postulated oxidative stress in severe malnutrition would result in induction of GSTs in erythrocytes. Erythrocyte GST activity towards 1-chloro-2,4-dinitrobenzene (CDNB) was measured in 271 malnourished children (22 undernourished; 92 marasmic; 82 kwashiorkor; 75 marasmic-kwashiorkor) and 48 healthy children. GST activity in the malnourished children was significantly higher than the control group (P < 0.01). The GST activity in the four classes of malnutrition did not differ. There was a weak relationship between GST activity and the height deficit, but not with the weight deficit, or the clinical features displayed by the children. The 11 children that died had a higher value than the survivors. There was no change in GST with anthropometric recovery. We conclude that erythrocyte GST has been induced in children with malnutrition. Induction of erythrocyte GST may be the result of exposure of the children to oxidative stress during the months prior to their presentation with severe malnutrition.