|Badaloo, Asha - UNIVERSITY OF WEST INDIES|
|Reid, Marvin - UNIVERSITY OF WEST INDIES|
|Forrester, Terrence - UNIVERSITY OF WEST INDIES|
Submitted to: American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: July 20, 2009
Publication Date: December 14, 2006
Citation: Jahoor, F., Badaloo, A., Reid, M., Forrester, T. 2006. Sulfur amino acid metabolism in children with severe childhood undernutrition: Cysteine kinetics. American Journal of Clinical Nutrition. 84(6):1393-1399. Interpretive Summary: It is believed that the organs of severely malnourished children malfunction because harmful compounds called oxidants injure the tissues in these organs. In a healthy person oxidants are made harmless because another compound called glutathione neutralizes them. Glutathione is made from three amino acids that we get from the protein we eat in our food. We found that malnourished children were not making enough glutathione because they lacked one of these amino acids called cysteine. The body is supplied with cysteine made from another amino acid called methionine, from our diet and when our body proteins are broken down. In this study we wanted to find out why children with a form of malnutrition called kwashiorkor were not getting enough cysteine to make glutathione. We found that these children were able to make some cysteine from methionine but they produced less cysteine because they were breaking down their body proteins at a much slower rate than when they were not malnourished. This finding suggests that supplements of cysteine may be needed to help prevent damage to the organs of malnourished patients.
Technical Abstract: Children with edematous but not nonedematous severe childhood undernutrition (SCU) have lower plasma and erythrocyte-free concentrations of cysteine, the rate-limiting precursor of glutathione synthesis. We propose that these lower cysteine concentrations are due to reduced production secondary to slower de novo synthesis plus decreased release from protein breakdown. We aimed to measure cysteine production, de novo synthesis, and the rate of cysteine release from protein breakdown in children with SCU. Cysteine flux, de novo synthesis, and release from protein breakdown were measured in 2 groups of children with edematous (n = 11) and nonedematous (n = 11) SCU when they were infected and malnourished (clinical phase 1), when they were still severely malnourished but no longer infected (clinical phase 2), and when they had recovered (clinical phase 3). In clinical phase 1, cysteine production and its release from protein breakdown were slower in both groups of children than were the values in the recovered state. These kinetic variables were significantly slower, however, in the children with edematous SCU than in those with nonedematous SCU. De novo cysteine synthesis in clinical phase 1 was faster than the rate at recovery in the edematous SCU group, and there were no significant differences between the groups at any clinical phase. These findings suggest that cysteine production is reduced in all children with SCU because of a decreased contribution from protein breakdown and not from decreased de novo synthesis. The magnitude of this reduction, however, is much greater in children with edematous SCU than in those with nonedematous SCU.