scholarly journals 17β-Estradiol Promotes Apoptosis of HepG2 Cells Caused by Oxidative Stress by Increasing Foxo3a Phosphorylation

2021 ◽  
Vol 12 ◽  
Author(s):  
Yusheng Guo ◽  
Xiangsheng Cai ◽  
Hanwei Lu ◽  
Qiqi Li ◽  
Ying Zheng ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Hepatocellular Carcinoma ◽  
Superoxide Dismutase ◽  
Hepg2 Cells ◽  
Manganese Superoxide Dismutase ◽  
Manganese Superoxide ◽  
B Virus ◽  
17Β Estradiol ◽  
New Treatment

Liver cancer is associated with high mortality, particularly in patients infected with the hepatitis B virus. Treatment methods remain very limited. Here, we explored the effects of 17β-estradiol (E2) on apoptosis of various liver cell lines (LO2, HepG2, and HepG2.2.15 cells). Within a certain concentration range, 17β-estradiol induced oxidative stress and apoptosis of HepG2 cells, downregulated ERα-36 expression, and increased Akt and Foxo3a phosphorylation. p-Foxo3a became localized around the nucleus but did not enter the organelle. The levels of mRNAs encoding manganese superoxide dismutase (MnSOD) and catalase, to the promoters of which Foxo3a binds to trigger gene expression, were significantly reduced in HepG2 cells. 17β-estradiol had no obvious effects on LO2 or HepG2.2.15 cells. We speculate that 17β-estradiol may induce oxidative stress in HepG2 cells by increasing Foxo3a phosphorylation, thus promoting apoptosis. This may serve as a new treatment for hepatocellular carcinoma.

Rat lung antioxidant enzymes: differences in perinatal gene expression and regulation

1992 ◽  
Vol 263 (4) ◽  
pp. L466-L470 ◽  
Author(s):  
L. B. Clerch ◽  
D. Massaro
Keyword(s):  
Gene Expression ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Manganese Superoxide Dismutase ◽  
Late Gestation ◽  
Postnatal Exposure ◽  
Sod Activity ◽  
Copper Zinc Superoxide Dismutase ◽  
Manganese Superoxide ◽  
Copper Zinc

The lung activity of the antioxidant enzymes (AOEs) copper, zinc superoxide dismutase (Cu,Zn SOD), catalase (CAT), and glutathione peroxidase (GP), but not manganese superoxide dismutase (Mn SOD), increases in rats during late gestation; the concentrations of Cu,Zn SOD mRNA and CAT mRNA also rise. During early postnatal exposure to > 95% O2, the lung activity of Cu,Zn SOD, CAT, and GP increases. We now show 1) the lung concentration of Mn SOD mRNA and GP mRNA does not increase in late gestation; 2) Mn SOD activity and the concentration of its mRNA and of GP mRNA increase during exposure of neonatal rats to > 95% O2; and 3) as previously shown for CAT mRNA, the increase in lung concentration of the mRNAs for Cu,Zn SOD, Mn SOD, and GP during early postnatal hyperoxia occurs with a 70–80% prolongation of the half-life of these mRNAs. We conclude that 1) in late gestation the level at which lung AOE gene expression is regulated differs among the enzymes, 2) the level at which lung AOE gene expression is regulated shortly after birth in response to > 95% O2 is uniform among the enzymes, and 3) the lung's AOE response to neonatal hyperoxia is not merely a step-up of its prenatal regulation but involves different regulatory mechanisms based on increased stability of AOE mRNAs

scholarly journals Role of reduced manganese superoxide dismutase in ischemia-reperfusion injury: a possible trigger for autophagy and mitochondrial biogenesis?

2013 ◽  
Vol 304 (3) ◽  
pp. F257-F267 ◽  
Author(s):  
Nirmala Parajuli ◽  
Lee Ann MacMillan-Crow
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Renal Function ◽  
Mitochondrial Biogenesis ◽  
Renal Damage ◽  
Manganese Superoxide Dismutase ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Manganese Superoxide ◽  
Oxidant Production

Excessive generation of superoxide and mitochondrial dysfunction has been described as being important events during ischemia-reperfusion (I/R) injury. Our laboratory has demonstrated that manganese superoxide dismutase (MnSOD), a major mitochondrial antioxidant that eliminates superoxide, is inactivated during renal transplantation and renal I/R and precedes development of renal failure. We hypothesized that MnSOD knockdown in the kidney augments renal damage during renal I/R. Using newly characterized kidney-specific MnSOD knockout (KO) mice the extent of renal damage and oxidant production after I/R was evaluated. These KO mice (without I/R) exhibited low expression and activity of MnSOD in the distal nephrons, had altered renal morphology, increased oxidant production, but surprisingly showed no alteration in renal function. After I/R the MnSOD KO mice showed similar levels of injury to the distal nephrons when compared with wild-type mice. Moreover, renal function, MnSOD activity, and tubular cell death were not significantly altered between the two genotypes after I/R. Interestingly, MnSOD KO alone increased autophagosome formation, mitochondrial biogenesis, and DNA replication/repair within the distal nephrons. These findings suggest that the chronic oxidative stress as a result of MnSOD knockdown induced multiple coordinated cell survival signals including autophagy and mitochondrial biogenesis, which protected the kidney against the acute oxidative stress following I/R.

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