PEROXISOMES AND THE HEPATIC PATHOLOGY OF CHILDHOOD MALNUTRITION

Liver specimens obtained immediately after death from eight severely m alnourished children were examined by electron microscopy, and compare d with seven liver biopsy specimens from children who had recovered fr om malnutrition. The liver cells from the fatal cases showed mitochond rial swelling, with coarse densities in the matrix, cholestasis, deple tion of the endoplasmic reticulum and Golgi apparatus, diminished glyc ogen stores, prominent lipid deposits and focal cytoplasmic degradatio n. The nucleoli were enlarged. There was marked reduction in peroxisom es. In contrast, the biopsies from recovering children showed good cel lular organisation, and a normal frequency of peroxisomes. Multiple fa ctors, including sepsis, may lead to depletion of peroxisomes. Loss of peroxisomes may interrupt beta-oxidation of long-chain fatty acids an d accentuate the accumulation of lipid. Moreover, a reduction in the c oncentration of catalase may remove one avenue for the detoxification of free radicals. As the concentration of other anti-oxidants, notably glutathione, is also reduced, free radical damage may occur, leading to lipid peroxidation of membranes, mitochondrial damage, pump failure and influx of water and electrolytes into the cell.