Abstract
Accumulating evidence has reported that nitric oxide (NO) can be cytotoxic and induce apoptosis. NO can also be genotoxic and cause DNA damage and mutations. It has been shown that NO damages mitochondrial DNA (mtDNA) to a greater extent than nuclear DNA. Sodium Nitroprusside (SNP), a NO donor, could efficiently promote NO formation. The viability of retinal ganglion cells (RGC) and the mtDNA copy numbers could also be altered by SNP conduction. Mitochondrial transcription factor A (TFAM), an mtDNA transcription factor, plays an essential role in the maintenance of mtDNA and mitochondrial homeostasis. The expression of TFAM was up-regulated by low dose SNP while down-regulated by high dose SNP. TFAM overexpression attenuated the regulatory effect of SNP on RGC viability and mtDNA numbers, while TFAM inhibition even amplified the regulatory effect of SNP. Moreover, the expression of apoptosis-related proteins in the mitochondria, Bcl-2 and Bax, were both altered by SNP treatment. These results suggested that TFAM impacted in SNP regulation of RGC viability and mtDNA numbers through the mitochondria-dependent pathway mediated by Bcl-2 and Bax subfamily.
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