Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes.

Patel, Tushar; Bronk, Steven F.; Gores, Gregory J.

doi:10.1172/jci117579

Cited by 258 publications

(184 citation statements)

References 55 publications

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“…Mg 2 þ mobilization is an early event in Fas-mediated apoptosis in B cells 31 and in glycodeoxycholate-induced apoptosis in rat hepatocytes. 32 An increase in free cytosolic Mg 2 þ facilitates the BID-or Bax-mediated release of cytochrome c from the mitochondria. 31,33 Thus, binding of Mg 2 þ by Tf may contribute to the antiapoptotic effects of Tf.…”

Section: Discussionmentioning

confidence: 99%

Prevention of Fas-mediated hepatic failure by transferrin

Lesnikov

Lesnikova

Shulman

et al. 2004

Laboratory Investigation

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Recent studies in lymphohemopoietic cells show that transferrin (Tf), a pivotal component of iron transport and metabolism, also exerts cytoprotective functions. We show here in a murine model that Tf interferes with Fasmediated hepatocyte death and liver failure. The mechanism involves the downregulation of apoptosis via BID, cytochrome c, caspase-3 and caspase-9, and upregulation of antiapoptotic signals via Bcl-xL. The results obtained with iron-saturated Tf, Apo-Tf and the iron-chelator salicylaldehyde isonicotinoyl hydrazone indicate that the observed antiapoptotic effect of Tf was not mediated by iron alone. In conclusion, the data suggest that Tf has broader functions than previously recognized and may serve as a cytoprotective agent.

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Section: Discussionmentioning

confidence: 99%

Prevention of Fas-mediated hepatic failure by transferrin

Lesnikov

Lesnikova

Shulman

et al. 2004

Laboratory Investigation

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“…Nuclear changes indicative of apoptosis were quantitated using fluorescent microscopy and the nuclear fluorescent binding dye 4,6-diamidino-2-phenylindole (DAPI) as we have previously described in detail (37)(38)(39). Results were confirmed by confocal microscopy.…”

Section: Methodsmentioning

confidence: 99%

“…Results were confirmed by confocal microscopy. DNA was isolated from cultured cells and separated by agarose gel electrophoresis as we have also previously described in detail (18,38).…”

Section: Methodsmentioning

confidence: 99%

Selective induction of apoptosis in Hep 3B cells by topoisomerase I inhibitors: evidence for a protease-dependent pathway that does not activate cysteine protease P32.

Adjei¹,

Kaufmann²,

Leung³

et al. 1996

J. Clin. Invest.

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“…Membrane lipid peroxidation can induce damage, including transition in permeability and release of apoptotic factors that lead to cell death (Mattson 1998). Hydrophobic bile acids induce apoptosis in rat hepatocytes (Patel et al 1994). It is known that apoptotic changes occur in hepatocytes during primary biliary cirrhosis (Kuroki et al 1996).…”

Section: Discussionmentioning

confidence: 99%

“…Patel et al (1994) reported that hydrophobic bile acids caused apoptosis of rat hepatocytes. It has been suggested that hepatotoxicity induced by hydrophobic bile acids is associated with cholestatic change (Strange et al 1979;Attili et al 1986;Hofmann 1990).…”

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confidence: 99%

Ebselen Protects against the Reduction in Levels of Drug‐Metabolizing Enzymes in Livers of Rats with Deoxycholic Acid‐Induced Liver Injury

Tanaka

Takezawa

Kumai

et al. 2002

Pharmacology & Toxicology

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Ebselen is a seleno-organic compound that inhibits oxidative stress by lipid peroxidation through a glutathione peroxidase-like activity. We studied the effect of ebselen on the expression of hepatic drug-metabolizing enzymes in rats with deoxycholic acid-induced liver injury. Hydrophobic bile acids, such as deoxycholic acid, are known to cause cholestatic liver injury, and it was reported that expression of hepatic cytochrome P-450 (CYP) was reduced by deoxycholic acid administration in rats. Hydrophobic bile acids induce lipid peroxidation in the liver, and this may be one mechanism of the development of liver injury. In the present study, we investigated the effect of ebselen (30 mg/kg/day for 10 days) on rats ingesting deoxycholic acid (1% of diet for 10 days). Deoxycholic acid decreased levels of CYP1A1, 2B1, 2E1 and 3A2 to 34, 58, 62 and 37% of control values, respectively, and increased serum alkaline phosphatase (ALP) and alanine aminotransferase (ALT) activities to 1.8 and 8.6 times the levels of controls, respectively. Administration of ebselen with deoxycholic acid prevented the decreases in levels of CYP1A1 and 3A2 (86 and 65% of control, respectively) and the increases in serum ALP and ALT activities (1.4 and 1.9 times of control, respectively) caused by deoxycholic acid. These results indicate that ebselen may have a protective effect against hydrophobic bile acid-induced liver injury.

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Increases of intracellular magnesium promote glycodeoxycholate-induced apoptosis in rat hepatocytes.

Abstract: Invest. 1994Invest. . 94:2183Invest. -2192

Cited by 258 publications

References 55 publications

Prevention of Fas-mediated hepatic failure by transferrin

Prevention of Fas-mediated hepatic failure by transferrin

Selective induction of apoptosis in Hep 3B cells by topoisomerase I inhibitors: evidence for a protease-dependent pathway that does not activate cysteine protease P32.

Ebselen Protects against the Reduction in Levels of Drug‐Metabolizing Enzymes in Livers of Rats with Deoxycholic Acid‐Induced Liver Injury

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