The study showed that Se and Zn supplementation might be beneficial in preventing biochemical alterations and neurobehavioral deficits in PM children.

The effect of the liver mitogen, lead nitrate [Pb(NO3)2], on protein-undernutrition-induced increased lipid peroxidation and reduced antioxidants levels was investigated in rats. Animals were divided into four groups: A, B, C, and D of five animals each. Animals in groups C and D were placed on a low-protein diet (5% casein) and animals in groups A and B were maintained on a normal diet (16% casein) for 14 wk and fed ad libitum. Animals in groups B and D were each given a single intravenous injection of Pb(NO3)2 (100 micromol/kg body weight) 72 h before sacrifice. The results confirm that protein undernutrition (PU) induced an increase in lipid peroxidation with concomitant reductions in catalase (CAT) activity, glutathione (GSH) level, and superoxide dismutase (SOD) activity. Lead (Pb) treatment, however, provoked increased lipid peroxidation, CAT activity, and GSH level but resulted in reduced SOD activity in both normal and PU-rats. These results suggest that Pb exacerbates liver lipid peroxidation in PU rats and suggests the involvement of free radicals in the pathogenesis of Pb poisoning. In addition, the results show that Pb affects well-fed and PU rats in similar ways but that the CAT activity of PU rats is more sensitive to the effect of Pb than that of normal rats.

Postnatal protein-undernutrition impacts on mental development and cognition in children and can lead to problem with attention and unresponsiveness which compromise children's ability to learn. These behavioral disorders might be due to alteration in calcium homeostasis as calcium plays critical roles in fundamental functions of neuron. The role of low protein diet as well as Se and Zn supplementation on intracellular calcium concentration ([Ca(2+)]i), Ca(2+)-ATPase, Na(+)-K(+)-ATPase, calpain and caspase-3 activities from rat cortex and cerebellum were investigated. Well-fed (WF) and low protein diet-fed (LPDF) rats were given diets containing 16% and 5% casein, respectively, for a period of 10 weeks. Then, the rats were supplemented with Se and Zn at a concentration of 0.15 mgL(-1) and 227 mgL(-1), respectively, in drinking water for 3 weeks. The results obtained from the study showed a significant increase in [Ca(2+)]i; calpain and caspase-3 activities as well as increase transfer latency in water maze study and reductions in Ca(2+)-ATPase and Na(+)-K(+)-ATPase activities for LPDF rats compared to WF rats. Se and Zn supplementation to LPDF rats reversed the elevation in [Ca(2+)]i, calpain and caspase-3 activities and restored the cognitive deficits and the activities of Ca(2+)-ATPase and Na(+)-K(+)-ATPase. Conclusively, protein-undernutrition results in the accumulation of synaptosomal calcium and inhibition of calcium transporters presumably via free radical generations and results in cognitive impairment which also probably results from neuronal death in rats through calpain activation and the caspase cascade mechanisms. However, Se and Zn supplementations ameliorated the anomalies observed.

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