Roles of Se and NO in apoptosis of hepatoma cells

Liu, Shanlin; Shia, Dongyun; Liu, Guanzhong; Chen, Huili; Liu, Shijin; Hu, Yun

doi:10.1016/s0024-3205(00)00960-7

Cited by 25 publications

(14 citation statements)

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“…Selenium compounds have hepato-protective effects against different types of oxidative stress [77,78] and decrease DNA damage [79] and can induce apoptosis in hepatoma cells [80]. It is difficult to obtain any meaningful conclusion from the two studies which measured selenium content in HCC with one study [81] showing a statistically significant decrease in selenium content in HCC compared to surrounding tissues and the other study [53] finding no significant difference in the selenium levels between HCC and surrounding tissues or normal controls.…”

Section: Discussionmentioning

confidence: 99%

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Trace Element Concentration in Primary Liver Cancers—A Systematic Review

Gurusamy

2007

Biol Trace Elem Res

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Section: Discussionmentioning

confidence: 99%

“…Selenium compounds have hepato-protective effects against different types of oxidative stress [77,78] and decrease DNA damage [79] and can induce apoptosis in hepatoma cells [80]. Some studies have reported a lower level of selenium in HCC than that of surrounding tissues [81], while others have not demonstrated this [53].…”

mentioning

confidence: 99%

Trace Element Concentration in Primary Liver Cancers—A Systematic Review

Gurusamy

2007

Biol Trace Elem Res

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“…Thapsigargin-induced cell death was not significantly suppressed in the presence of caspase-3 inhibitor or NAME. NO may be important as a signaling factor in many cells [Lowenstein et al, 1994], and it plays a role in apoptosis of hepatoma cells [Liu et al, 2000]. NO mediates apoptosis by D-galactosamine in a primary culture of rat hepatocytes [Abou-Elella et al, 2002].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of regucalcin suppresses apoptotic cell death in cloned normal rat kidney proximal tubular epithelial NRK52E cells: Change in apoptosis‐related gene expression

Nakagawa

Yamaguchi

2005

J of Cellular Biochemistry

101

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The effect of regucalcin, a regulatory protein in intracellular signaling pathway, on cell death and apoptosis was investigated using the cloned normal rat kidney proximal tubular epithelial NRK52E cells overexpressing regucalcin. NRK52E cells (wild type) and stable regucalcin (RC)/pCXN2 transfectants were cultured for 72 h in a medium containing 5% bovine serum (BS) to obtain subconfluent monolayers. After culture for 72 h, cells were further cultured for 24-72 h in a medium without BS containing either vehicle, tumor necrosis factor-alpha (TNF-alpha; 0.1 or 1.0 ng/ml of medium), lipopolysaccharide (LPS; 0.1 or 1.0 microg/ml), Bay K 8644 (10(-9)-10(-7) M), or thapsigargin (10(-9)-10(-7) M). The number of wild-type cells was significantly decreased by culture for 42-72 h in the presence of TNF-alpha (0.1 or 1.0 ng/ml), LPS (0.1 or 1.0 microg/ml), Bay K 8644 (10(-7)-10(-5) M), or thapsigargin (10(-8) or 10(-7) M). The effect of TNF-alpha (0.1 or 1.0 ng/ml), LPS (0.1 or 1.0 microg/ml), Bay K 8644 (10(-7)-10(-6) M), or thapsigargin (10(-7) M) in decreasing the number of wild-type cells cultured for 24-72 h was significantly prevented in transfectants overexpressing regucalcin. Agarose gel electrophoresis showed the presence of low-molecular-weight deoxyribonucleic acid (DNA) fragments of adherent wild-type cells cultured with LPS (1.0 microg/ml), Bay K 8644 (10(-7) M), or thapsigargin (10(-8) M) for 24 h, and this DNA fragmentation was significantly suppressed in transfectants. DNA fragmentation in adherent cells was not seen by culture with TNF-alpha (1.0 ng/ml). TNF-alpha-induced decrease in the number of wild-type cells was significantly prevented by culture with caspase-3 inhibitor (10(-8) M), while LPS- or Bay K 8644-induced decrease in cell number was significantly prevented by caspase-3 inhibitor or N omega-nitro-L-arginine methylester (NAME) (10(-5) M), an inhibitor of nitric oxide (NO) synthase. Thapsigargin-induced decrease in cell number was not prevented in the presence of two inhibitors. Bcl-2 and Akt-1 mRNA levels were significantly increased in transfectants cultured for 24 h as compared with those of wild-type cells, while Apaf-1, caspase-3, or glyceroaldehyde-3-phosphate dehydrogenase (G3PDH) mRNA expressions were not significantly changed in transfectants. Culture with TNF-alpha (1.0 ng/ml), LPS (1.0 microg/ml), Bay K 8644 (l0(-7) M), or thapsigargin (10(-8) M) caused a significant increase in caspase-3 mRNA levels in wild-type cells. LPS (1.0 microg/ml) significantly decreased Bcl-2 mRNA expression in the cells. Their effects on the gene expression of apoptosis-related proteins were not significantly changed in transfectants. This study demonstrates that overexpression of regucalcin has a suppressive effect on cell death and apoptosis induced by various factors which their action are mediated through many intracellular signaling pathways, and that it modulates the gene expression of apoptosis-related proteins.

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“…GSH-Px, as a Secontaining enzyme, can scavenge free radicals through glutathione and repress the chain reaction of lipid peroxidation, and its activity is affected by the level of intake of selenium (Zhao et al, 2008). Se-containing polysaccharide from Krestin (Se-PSK) can effectively increase the anti-oxidant activity by improving the activity of GSH-Px and superoxide dismutase (SOD) and decreasing the content of lipid peroxide, thus preventing or alleviating the injury from lipid peroxidation (Liu et al, 2000;Zhang et al, 2005a). Selenium-containing polysaccharide from Cardamine UrbanianaO.…”

Section: Introductionmentioning

confidence: 99%

“…Selenoastragalan (Se-AMP), an organic selenium compound combining astragalus membranaceus polysaccharide (AMP) with trace element selenium might not only promote the tumor inhibitory effects of AMP but also bring antioxidant activity of Se into full play by reducing the contents of lipid peroxide in plasma to exert significant tumorinhibitory effects in sarcoma bearing mice (Gong, 1996). Liu et al have proved that Se-containing polysaccharides can elevate both the GSH-Px activity in mouse blood and the content of nitric oxide (NO) both in mouse plasma and the hepatoma cell (H22) culture (Liu et al, 1998). It was speculated that the inhibition of tumor tissue and cell growth by Se-containing polysaccharides was possibly related to the elevation of the activity of GSH-Px and the capability of scavenging free oxygen radicals.…”

Section: Introductionmentioning

confidence: 99%

Antitumor mechanism of Se-containing polysaccharide, a novel organic selenium compound

Shang

Cui

et al. 2009

Front. Biol. China

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Recent studies on the inhibition of tumor growth by Se-containing polysaccharide were reviewed. Meanwhile, the possible molecular mechanisms of the inhibition of tumor cell growth through antioxidation, induction of tumor cell apoptosis, blockade of cell cycle, and enhancement of immunity by Se-containing polysaccharide were proposed. In the end, the potential application of Se-containing polysaccharide in the prevention and treatment of tumor was elucidated.

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Roles of Se and NO in apoptosis of hepatoma cells

Cited by 25 publications

References 0 publications

Trace Element Concentration in Primary Liver Cancers—A Systematic Review

Trace Element Concentration in Primary Liver Cancers—A Systematic Review

Overexpression of regucalcin suppresses apoptotic cell death in cloned normal rat kidney proximal tubular epithelial NRK52E cells: Change in apoptosis‐related gene expression

Antitumor mechanism of Se-containing polysaccharide, a novel organic selenium compound

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