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Apoptosis initiated by carbon tetrachloride in mitochondria of rat primary cultured hepatocytes

	author = {Yan Cai and Li-kun Gong and Xin-ming Qi and Xiang-hong Li and Jin Ren},
	title = {Apoptosis initiated by carbon tetrachloride in mitochondria of rat primary cultured hepatocytes},
	journal = {Acta Pharmacologica Sinica},
	volume = {26},
	number = {8},
	year = {2016},
	keywords = {},
	abstract = {Aim: To investigate the mitochondria-initiated apoptosis pathway involved in Carbon tetrachloride (CCl4) hepatotoxicity in vitro.
Methods: Several cytotoxicity endpoints, including WST-8 metabolism, lactate dehydrogenase leakage and morphological changes, were examined. The 5,5'-dithio-bis(2-nitrobenzoic acid) reaction was used to measure reduced glutathione level, and the malondialdehyde level was determined using the thiobarbituric acid assay. The release of cytochrome c and Bcl-XL was detected by Western blot. Caspase-3 activity was measured using the fluorogenic substrate Ac-DEVD-AMC. DNA fragmentation was used to evaluate cell apoptosis.
Results: A time-and dose-dependent decrease in cellular glutathione content was observed, along with a concomitant increase in malondialdehyde levels following the application of CCl4. Caspase 3 activity was stimulated at all doses of CCl4, with the most significant activation at 3 mmol/L. Cytochrome c was released obviously after CCl4 treatment. A time-dependent decrease in Bcl-XL expression was observed. DNA fragmentation results revealed apoptosis and necrosis following CCl4 treatment.
Conclusion: Oxidative damage is one of the essential mechanisms of CCl4 hepatotoxicity, which triggers apoptosis via the mitochondria-initiated pathway.},
	issn = {1745-7254},	url = {}