Dietary factors in lipofuscinogenesis and ceroidogenesis

The presence of ceroid pigments in human and animal tissues is associated with numerous pathological conditions in which the main pathogenic factor is the primary or secondary deficiency of vitamin E or imbalances between anti- and pro-oxidants. That oxidative stress, particularly through its consequent lipid peroxidation, plays a capital role in the genesis of ceroid pigments, is supported by numerous in vitro and in vivo studies. Discussed in this presentation are two examples of oxidative stress on ceroidogenesis, namely the in vivo rat model of dietary hepatic necrosis, and the in vitro formation of ceroid pigments by the aerobic incubation of unsaturated fat and blood cells. Although it is widely believed that the progressive accumulation of lipofuscin is also a marker of oxidative stress, and that this pigment can be modulated by the dietary anti- and pro-oxidant factors, the evidence for these related notions is highly questionable. Some years ago, this controversial problem was reexplored in our laboratories by a series of studies in Wistar male rats, and the results indicated that neither the type of dietary fat, nor the pharmacological amounts of vitamin E significantly influenced the amounts of lipofuscin in cerebral neurons, cerebellar Purkinje cells, hepatocytes or cardiac myocytes. It was also found that the indices of lipid peroxidation determined in this study (production of malonaldehyde, and detection of conjugated dienes) did not correlate with the progressive accumulation of lipofuscin with age. All these results strongly suggest that the presence and cellular accumulation of lipofuscin can hardly be considered a marker of oxidative stress.