Inhibitory effect of D‐galactosamine administration on fatty acid oxidation in rat hepatocytes

Mangeney-Andreani, Marise; Sire, Olivier; Montagne-Clavel, Jacqueline; Nordmann, Roger; Nordmann, J

doi:10.1016/0014-5793(82)80180-4

Cited by 17 publications

(6 citation statements)

References 15 publications

(8 reference statements)

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“…Liver PL concentration was higher in galactosamine-injected rats than in controls 24 h after injec- tion but was lower at 72 h than in controls (Table 1). Galactosamine-injected rats therefore had fatty livers 24 and 48 h after injection, as described previously, probably because of decreased ␤-oxidation (25). ␣-TTP mRNA and protein contents were measured to elucidate the effect of galactosamine-induced acute liver injury on ␣-TTP synthesis.…”

Section: Resultsmentioning

confidence: 93%

Galactosamine-Induced Acute Liver Injury in Rats Reduces Hepatic .ALPHA.-Tocopherol Transfer Protein Production

Takenaka

Kita

Ikeya

et al. 2007

J Nutr Sci Vitaminol

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SummaryThe liver plays the main role in the secretion of food-derived ␣ -tocopherol into the circulation through the functioning of ␣ -tocopherol transfer protein ( ␣ -TTP). However, the effect of liver disease on ␣ -TTP level and ␣ -tocopherol metabolism has not been clarified. We examined the amount of liver ␣ -TTP and its effect on serum ␣ -tocopherol concentration in liver injury. Male Wistar rats were injected intraperitoneally with D -galactosamine at 800 mg/kg body weight, and liver and serum lipid concentrations, ␣ -tocopherol concentrations, and hepatic ␣ -TTP mRNA and protein levels were measured at 24, 48, and 72 h after injection. On the basis of body weight changes and serum transaminase activities, the livers were found to be in an injured state 24 and 48 h after galactosamine injection but had recovered by 72 h. The hepatic ␣ -TTP mRNA level was reduced throughout the experimental period, and at 48 h after injection the ␣ -TTP protein level had begun to decrease. Lipid and ␣ -tocopherol concentrations in the serum were decreased at 24 and 48 h after injection and increased at 72 h. Liver lipid concentrations were increased at 24 and 48 h after injection, but the liver ␣ -tocopherol concentration was unchanged. These results show that galactosamine-induced liver injury decreases hepatic ␣ -TTP synthesis in rats. Serum ␣ -tocopherol concentration was not directly affected by the acute change in hepatic ␣ -TTP level, suggesting that the chronic changes in ␣ -TTP activity would be necessary to regulate serum ␣ -tocopherol concentration.

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Section: Resultsmentioning

confidence: 93%

Galactosamine-Induced Acute Liver Injury in Rats Reduces Hepatic .ALPHA.-Tocopherol Transfer Protein Production

Takenaka

Kita

Ikeya

et al. 2007

J Nutr Sci Vitaminol

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“…[36][37][38] Excessive production of free radicals resulting from oxidative stress can damage such macromolecules as lipids.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Pinitol againstD-Galactosamine-Induced Hepatotoxicity in Rats Fed on a High-Fat Diet

Zhou

Park

Cho

et al. 2008

Bioscience, Biotechnology, and Biochemistry

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“…Studies from Quintero et al [47] showed that free radical dependent pathway is involved in GalN induced hepatic apoptosis and necrosis in rat hepatocytes. Mangeney-Andreani et al [10] suggested that energy metabolism of hepatocytes was also inhibited by GalN application. In addition, report from Sire et al [48] reveals that GalN damaged the enzymes involved in the transport of substrates to the mitochondria and consequently modified the phospholipid composition of the membrane.…”

Section: Discussionmentioning

confidence: 99%

Amelioration of galactosamine-induced nephrotoxicity by a protein isolated from the leaves of the herb, Cajanus indicus L

Sinha

Manna

Sil

2007

BMC Complement Altern Med

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BackgroundGalactosamine (GalN), an established experimental toxin, mainly causes liver injury via the generation of free radicals and depletion of UTP nucleotides. Renal failure is often associated with end stage liver damage. GalN intoxication also induces renal dysfunction in connection with hepatic disorders. Present study was designed to find out the effect of a protein isolated from the leaves of the herb Cajanus indicus against GalN induced renal damage.MethodsBoth preventive as well as curative effect of the protein was investigated in the study. GalN was administered intraperitoneally at a dose of 800 mg/kg body weight for 3 days pre and post to protein treatment at an intraperitoneal dose of 2 mg/kg body weight for 4 days. The activities of antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione-S-transferase (GST), levels of cellular metabolites, reduced glutathione (GSH), total thiols, oxidized glutathione (GSSG) and lipid peroxidation end products were determined to estimate the status of the antioxidative defense system. In addition, serum creatinine and urea nitrogen (UN) levels were also measured as a marker of nephrotoxicity.ResultsResults showed that GalN treatment significantly increased the serum creatinine and UN levels compared to the normal group of mice. The extent of lipid peroxidation and the level of GSSG were also enhanced by the GalN intoxication whereas the activities of antioxidant enzymes SOD, CAT, GR and GST as well as the levels of total thiols and GSH were decreased in the kidney tissue homogenates. Protein treatment both prior and post to the toxin administration successfully altered the effects in the experimental mice.ConclusionOur study revealed that GalN caused a severe oxidative insult in the kidney. Protein treatment both pre and post to the GalN intoxication could protect the kidney tissue against GalN induced oxidative stress. As GalN induced severe hepatotoxicity followed by renal failure, the protective role of the protein against GalN induced renal damages is likely to be an indirect effect. Since the protein possess hepatoprotective activity, it may first ameliorate GalN-induced liver damage and consequently the renal disorders are reduced. To the best of our knowledge, this is probably the first report describing GalN-induced oxidative stress in renal damages and the protective role of a plant protein molecule against it.

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Inhibitory effect of D‐galactosamine administration on fatty acid oxidation in rat hepatocytes

Cited by 17 publications

References 15 publications

Galactosamine-Induced Acute Liver Injury in Rats Reduces Hepatic .ALPHA.-Tocopherol Transfer Protein Production

Galactosamine-Induced Acute Liver Injury in Rats Reduces Hepatic .ALPHA.-Tocopherol Transfer Protein Production

Protective Effect of Pinitol againstD-Galactosamine-Induced Hepatotoxicity in Rats Fed on a High-Fat Diet

Amelioration of galactosamine-induced nephrotoxicity by a protein isolated from the leaves of the herb, Cajanus indicus L

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