Developmental changes in the peroxidation potential of rat brain homogenate and mitochondria

Abstract

Lipid peroxidation, one of the most common expressions of oxidative stress, may be altered during normal physiological states including development. We have examined the changes in lipid peroxidation in rat brain, a tissue highly susceptible to oxidative damage, during this physiological state. In vivo lipid peroxidation was moderate in the foetal and neonatal period and increased during the postnatal development. Lipid peroxidation potential in brain homogenate and mitochondria, in Tris-HCl buffer or with exogenous cofactors, such as ascorbate-Fe2+, NADPH ADP-Fe3+ and cumene hydroperoxide, showed significant changes during pre- and postnatal development. In general, brain as well as liver (used as a standard tissue for comparison) seem to have low peroxidation potential in the foetal and neonatal period which then increases at different rates during development to reach adult values at different days. The low peroxidation potential corresponds to the rapid phase of cell proliferation. These results taken together with similar earlier finding in other systems may indicate a possible occurrence of a 'permissible period' during which the low levels of lipid peroxidation may be able to yield only low amounts of cytostatic aldehydes and peroxides as byproducts, thereby allowing rapid proliferation of cells.