Erythrocyte clutathione reductase activity and riboflavin status in severely malnourished children - abstract

Erythrocyte glutathione reductase (EGR), cofactor is riboflavin (vit B2), functions together with glucose 6-phosphate dehydrogenase to maintain cellular levels of glutathione and thus the integrity of the erythrocyte. The compromised antioxidant status of severely malnourished children along with increased exposure to metabolic stress led us to postulate that EGR activity might be increased in malnutrition as a compensatory response to oxidative stress. We therefore measured EGR activity in 49 severly malnourished children on admission and again in 35 of these children at discharge. Erythocyte glutathione-reductase-activation-coefficient (ERGAC), an index of riboflavin status, was also assessed. Twenty-two healthy children served as controls (C). The malnourished group had significantly higher EGR activity (8.34 ñ 0.31 U/g Hb; mean ñ SEM) than the control group (6.63 ñ 0.23 U/g Hb). On admission, children with marasmus (M) had significantly higher EGR activities (8.95 ñ .046 U/g Hb) than children with marasmic kwashiorkor (MK: 8.08 ñ 0.67 U/g Hb) or kwashiorkor (K: 7.66 ñ 0.53 U/g Hb). At discharge, high levels of EGR were maintained in all groups. However, the kwashiorkor group showed a significant increase up to (10.37 + 0.41 U/g Hb). An EGRAC > 1.30 indicates riboflavin deficiency. Forty per cent of the controls as well as 50 percent of the malnourished children were deficient in riboflavin supplementation of the malnourished groups, the EGRAC fell to normal levels. We concluded (1) that EGR activity is increased in severly malnourished children; this may be as a result of increased metabolic stress, and (2) the riboflavine status of malnourished children improved significantly during their recovery (AU)

Erythrocyte glutathione-s-transferase in malnutrition and homozygous sickle cell disease - abstract

The glutathione-S-transferases (GST) are a group of enzymes actively involved in the detoxification of reactive xenobiotics that would otherwise initiate cell damage. Glutathione (GSH) is an important co-factor for this enzymic detoxification process. The low levels of red cell GSH associated with oedematous malnutrition suggest that these children are experiencing some form of oxidative stress. Similarly, the unstable haemoglobin associated with homozygous sickle-cell disease (HbSS) may mean that oxidative stress occurs in this disease state. GST activity is induced during oxidative stress. Hence its measurement should provide an estimate of this stress. Erythrocyte GST activity was therefore measured in three groups of children: (a) 41 severely malnourished children on admission and in 18 at discharge, (b) 24 children with HbSS and 60 age-matched controls (HbAA), and (c) 25 children living at a Kingston Place of Safety (POS). (The data are shown in a Table). We conclude that malnourished children and children with HbSS have significantly higher levels of red cell GST activity when compared with either control group (HbAA and POS). GST activity was slightly higher at discharge in the malnourished group. It is possible that GST activity is induced in malnutrition and HbSS because of increased oxidative stress (AU)

Vitamin E in malnutrition - abstract

Free radical generation in vivo occurs through the normal activity of some oxidative enzymes, through food contaminants, microbial products and during infections. The manifestations of oxidant damage are fatty liver, increased membrane permeability and haemolysis - all features of severe malnutrition. The major antioxidant that prevents free radical-induced peroxidation in lipids is Vitamin E. We have therefore measured Vit. E concentration in the plasma of 52 severely malnourished children on admission and again at discharge. Thus of the oedematous children, 83 percent had biochemical Vit. E deficiency. Two of these children died: they had 1.0 and 2.4 mg/l Vit. E and at post mortem grossly fatty livers. Low Vit. E status occurred in about half the marasmic children. Two who died had Vit. E levels of 3.7 mg/l with fatty liver and 5.5 mg/l without fatty liver. At recovery, most of the children had normal Vit. E levels. They remained low in 6 children (5 boys and 1 girl). The only 2 children with the sex-linked disorder G-6-PD deficiency (45 were tested) failed to show an increase in Vit. E with recovery. A third boy had a very low activity of 6-PGAD - the second enzyme in the hexose monophosphate shunt. Two boys were not tested. The girl had normal G-6-PD and 6-PGAD but developed osteomyelitis during recovery. Thus, it is likely that each of these children failed to achieve normal levels of Vit. E during recovery because of increased oxidant stress. We conclude that biochemical Vit. E deficiency is common in malnutrition, particularly oedematous malnutrition, and that Vit. E deficiency may play a role (together with deficiencies of other antioxidants) in the fatty liver and membrane cation leak seen in malnutrition. Vit. E status should be assessed in a larger series of children with G-6-PD deficiency (AU)