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Abstract
<p class="first" id="d14594334e67">Hyperhomocysteinemia (HHcy) has been implicated
in the development of neurodegenerative
conditions and mild cognitive disorders. Mitochondrial dysfunctions are the major
mechanisms involved in homocysteine (Hcy)-induced neurotoxicity. Although, hydrogen
sulfide has been reported as potent antioxidant, its effects on Hcy-induced mitochondrial
dysfunctions have not been studied. Therefore, the present study has been designed
to evaluate the protective effect of NaHS on Hcy-induced mitochondrial dysfunctions
in brain. NaHS supplementation decreased reactive oxygen species and nitrite levels
in the cortex and hippocampus of animals with HHcy. NaHS supplementation increased
the activity of mitochondrial electron transport chain components; NADH dehydrogenase,
cytochrome c oxidase and F0-F1 ATPase in the cortex and hippocampus of HHcy animals
along with in-gel activity of complex I - complex V in the mitochondria isolated from
the cortex and hippocampus of HHcy animals. Moreover, NaHS supplementation also increased
the mitochondrial complex I, II and IV mediated oxygen consumption rate in Hcy treated
mitochondria. NaHS administration prevented the Hcy-induced mitochondrial damage as
suggested by the decreased mitochondrial swelling in the cortex and hippocampus of
HHcy animals. NaHS supplementation decreased the activity of lactate dehydrogenase
isozymes (1-5) in the brain regions of HHcy animals. The expression of protein kinase
c δ was also decreased in the brain regions of HHcy animals following NaHS supplementation.
This was accompanied by reduced activity of caspase-3 indicating anti-apoptotic effect
of H2S. Taken together, the findings suggest that H2S supplementation ameliorates
Hcy-induced oxidative stress and mitochondrial dysfunctions suggesting H2S releasing
drugs may be a novel therapeutic approach to treat HHcy associated neurological disorders.
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