Rat liver lysosome membranes are enriched in α-tocopherol

Abstract

The subcellular distribution of alpha-tocopherol has been studied in rat liver. Lysosomal membranes were found to be considerably enriched in alpha-tocopherol with 6300 pmol/mg membrane protein, whereas mitochondrial membranes and microsomes contained 530 and 200 pmol/mg membrane protein, respectively. The 37-fold higher specific content of alpha-tocopherol in lysosomal membranes relative to homogenate indicates that lysosomes could be a target of cellular pathology in vitamin E deficiency states.

Haptoglobin Genotype-dependent Differences in Macrophage Lysosomal Oxidative Injury

“…However, lysosomal injury needs large amounts of redox iron or additional oxidative trigger, and as long as the oxidative stress is not overwhelmingly strong, lysosomes are typically resistant to oxidative damage (44). The finding that the membranes of rat liver lysosomes contain a 37-fold higher content of ␣-tocopherol compared with other cellular membranes supports the notion that lysosomes are under substantial oxidative stress and antioxidants are needed to protect lysosomes from oxidative damage (45).…”

Intracellular trafficking of vitamin E in hepatocytes: the role of tocopherol transfer protein

“…4). Interestingly, lysosomes are the intracellular organelle in which the highest tocopherol concentrations are found (13,41,42). In contrast to our observations, it was previously reported that the localization pattern of ec- topically expressed TTP is diffuse throughout the cells, and shifts to an endosomal punctate pattern only upon treatment with chloroquine or bafilomycin (19).…”

“…In many cell types, the vitamin accumulates primarily in lysosomes (13) and mitochondria (14), where high levels of oxidative stress are presumed to exist. Especially enigmatic are the paths for intracellular transport of vitamin E in hepatocytes, the cells that regulate whole-body distribution of tocopherol.…”

Altered vitamin E status in Niemann-Pick type C disease

“…Finally, modest supplementation with vitamin E has been reported to result in a mild improvement in motor performance in a mouse model of NPC disease ( 34 ). On the cellular level, it has been established that uptake of vitamin E occurs via endocytosis ( 35,36 ) and that a signifi cant portion of the vitamin is found in lysosomes ( 37 ). In light of these observations, we hypothesized that proper intracellular traffi cking of vitamin E (and in turn, adequate antioxidant protection) depends on timely egress from the lysosome and, therefore, on the functionality of NPC1/2.…”