Molecular role of catalase on oxidative stress-induced Ca(2+) signaling and TRP cation channel activation in nervous system.

BACKGROUND: Catalase catalyzes the reduction of H(2)O(2) to water and it can also remove organic hydroperoxides. Nervous system in body is especially sensitive to free radical damage due to rich content of easily oxidizible fatty acids and relatively low content of antioxidants including catalase. Recent studies indicate that reactive oxygen species actually target active channel function, in particular TRP channels. I review the effects of catalase on Ca(2+) signaling and on TRP channel activation in neuroglial cells such as microglia and substantia nigra. MATERIALS: Review of the relevant literature and results from recent our basic studies, as well as critical analyses of published systematic reviews were obtained from the pubmed and the Science Citation Index.
RESULTS: It was observed that oxidative stress-induced activations of TRPM2, TRPC3, TRPC5 and TRPV1 cation channels in neuronal cells are modulated by catalase, suggesting antioxidant-dependent activation/inhibition of the channels. I provide also, a general overview of the most important oxidative stress-associated changes in neuronal mitochondrial Ca(2+) homeostasis due to oxidative stress-induced channel neuropathies. Catalase incubation induces protective effects on rat brain mitochondrial function and neuronal survival. A decrease in catalase activity through oxidative stress may have an important role in etiology of Parkinson's disease and sensory pain.
CONCLUSION: The TRP channels can be activated by oxidative stress products, opening of nonspecific cation channels would result in Ca(2+) influx, and then elevation of cytoplasmic free Ca(2+) could stimulate mitochondrial Ca(2+) uptake. Catalase modulates oxidative stress-induced Ca(2+) influx and some TRP channels activity in neuronal cells.