Evaluation of oxidative stress during apoptosis and necrosis caused by d-galactosamine in rat liver

Sun, Fang; Hamagawa, Eri; Tsutsui, Chihiro; Sakaguchi, Naomi; Kakuta, Yuri; Tokumaru, Sadako; Kojo, Shosuke

doi:10.1016/s0006-2952(02)01420-x

Cited by 95 publications

(92 citation statements)

References 31 publications

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“…Variety of enzymatic and nonenzymatic antioxidants scavenge the free radicals to prevent the cell from oxidative damage. Therefore, these antioxidants are expected to be consumed by enhanced radical reactions (Sun et al, 2003). Significant decrease in the activity of tissue antioxidant defense system after intraperitoneal administration of D-GalN has already been reported (Anandan et al, 1998;Ravikumar et al, 2005).…”

Section: Discussionmentioning

confidence: 94%

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Abdulazeez

Devaki

2013

Pharmaceutical Biology

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Context: Lycopene is a phytonutrient under considerable investigation for its antioxidant benefits in treating diseases like cancer, cardiovascular diseases, osteoporosis and diabetes. Objective: This study explores the effect of lycopene against oxidative damage during experimental hepatitis, induced by D-galactosamine/lipopolysaccharide (D-GalN/LPS). Materials and methods: Experimental rats were pretreated with lycopene intraperitoneally for 6 d (10 mg/kg body weight/day) and then induced by D-GalN/LPS. After induction, the levels of lipid peroxides in serum and liver of control and experimental group of animals were measured. The activities of enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase and nonenzymatic antioxidants, such as reduced glutathione, vitamin C and vitamin E were also analyzed. The genotoxic effect of D-GalN/LPS was evaluated through the comet assay. Results: The elevated level of lipid peroxides induced by D-GalN/LPS was significantly (p50.05) reverted in lycopene pretreated animals. Lycopene administration restored (p50.05) the decreased activities of enzymatic and nonenzymatic antioxidant markers during D-GalN/LPS induction. The DNA strand breaks (72.3 mM) generated during D-GalN/LPS toxic injury was significantly reduced (35.5 mM) upon pretreatment with lycopene as observed by reduced tail movement in comet assay. Discussion and conclusion: There is no conclusive report about lycopene-assisted protection against free radical mediated toxic injury induced by D-GalN/LPS. Our findings reveal that lycopene effectively combated oxidative damage and protected antioxidant defense status of the cell. Pretreatment of lycopene also offers protection against the DNA damage and confirms the antioxidant nature of the phytonutreint against experimental hepatitis.

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Section: Discussionmentioning

confidence: 94%

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Abdulazeez

Devaki

2013

Pharmaceutical Biology

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“…21,23,24) Furthermore, it has been suggested that GalN induces serious oxidative stress in the rat liver, leading to apoptosis and necrosis. 25) In a previous study, we found that PPE hinders the development of GalN-induced hepatic damage by inhibiting alterations in liver TBARS and GSH levels. 7) In the present study, although liver TBARS levels between the GalN-treated groups were not found to be significantly different, RPE tended to lower the increased TBARS level in the liver homogenate (Table 1).…”

Section: )mentioning

confidence: 87%

Red Potato Extract Protects fromD-Galactosamine-induced Liver Injury in Rats

Han

Hashimoto

et al. 2006

Bioscience, Biotechnology, and Biochemistry

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The protective effects of red potato extract (RPE) as to liver damage were determined in D-galactosamine (GalN)-intoxicated rats. Increases in serum aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase activities, all of which were induced by GalN injection, decreased in RPE administered rats, suggesting that RPE acts as a functional food showing anti-hepatotoxicity.Key words: colored potato; anthocyanin; D-galactosamine; hepatotoxicity; rat It is well-known that polyphenols originating from various fruits and vegetables have a wide range of biological effects such as antioxidant, anti-inflammatory, and anti-carcinogenic activities.1,2) Generally, potato has not been regarded as a food rich in antioxidants, but several researchers have found that depending on the genetic variety, some potato contain considerable amounts of polyphenols, flavonoids, and anthocyanins.3,4) Furthermore, recently new varieties of potato have been developed around the world to find new uses, as these are rich in antioxidants. Among new potatoes, the colored potato especially has attracted special interest in many countries due to its color appeal, such as yellow, purple, or red. The pigments of colored potatoes have been identified as anthocyanin derivatives.3-6) Like natural antioxidants from other plants, antioxidants from potato are believed to behave as an important functional food, 4) but little information is available. Recently, we found that purple potato extract (PPE, Hokkai no.92) attenuates the liver damage induced by D-galactosamine (GalN) in rats, 7) but it has not yet been reported that different colored potato extracts have analogous health benefits. Hence in this study we investigated the hepatoprotective effects of red potato extract (RPE, Hokkai no.91) against GalNinduced liver injury in rats.RPE was prepared according to our previous report. 7)Briefly, pared potato was homogenized with 5% formic acid and centrifuged at 2;000 Â g for 20 min at 4 C. Finally, the supernatant fraction was lyophilized and dissolved in 70% ethanol or distilled water (RPE). The total polyphenol content in the ethanol solution was determined by the Folin-Ciocalteu method.8) Absorbance was measured at 750 nm using a spectrophotometer (Shimadzu 1600-UV, Kyoto, Japan). The flavonoid content in the ethanol solution was determined according to the report of Jia et al., 9) using standards based on the known (+)-catechin concentration. Briefly, 200 ml of a known concentration of extract was mixed with 1.25 ml of distilled water and 75 ml of 5% NaNO 2 , and then 150 ml of 10% AlCl 3 was added 6 min later. Next, 500 ml of 1 N NaOH was added, and the total was made up to 2.5 ml with distilled water. Absorbance was measured at 510 nm using a spectrophotometer. The monomeric anthocyanin content in aqueous solution was measured by a pH differential method using a spectrophotometer.10) It was calculated using the molar extinction coefficient of pelargonidin-3-glucoside (31,600 l cm À1 mg À1 ), a molecular weight of 433.2 g mol À...

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“…Because TNF-␣ was suggested to mediate the development of GalN-hepatitis (6, 7) and Wallach et al (27) reported that preceding administration of TNF-␣ caused desensitization of mice to a lethal amount of TNF-␣, it would be likely that CBH desensitized the rats against GalN in the present study. The concentration of UDP-galactosamine in the liver of the rats increased rapidly after the injection of GalN (7)(8)(9)(10), and since the increase was accompanied by a reduction in the concentration of UTP and UDP-glucose in the liver, it is likely that the hepatotoxic action of GalN is mediated by suppression of RNA or glycoprotein biosynthesis caused by the deficiency of UTP or related compounds. Bauer et al (28) have reported inhibition of overall protein and glycoprotein secretion by GalN, and that was partially explained by inhibition of de novo protein synthesis.…”

Section: Discussionmentioning

confidence: 99%

“…Endotoxin is a constituent of the cell wall of gram-negative bacteria, and since it may be absorbed from the gastrointestinal tract into the portal venous circulation, the intestinal microflora have generally been considered to be important for the development of GalN-hepatitis. The induction of GalN-hepatitis has recently been suggested to be initialized by apoptosis, which would be caused by cytotoxic cytokines released from Kupffer cells by the stimulation of endotoxin or bacteria translocated from the digestive tract ( 8,9 ). On the other hand, GalN is thought to induce hepatotoxicity by inhibiting the synthesis of RNA and protein in the liver by decreasing intracellular UTP concentration, which finally leads to the necrosis of liver cells ( 5 , 10-12 ).…”

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confidence: 99%

Effects of Dietary Corn Bran Hemicellulose and Neomycin on Hepatic Caspase-3 Activity and Glycoprotein Concentration in Rats Treated with or without D-Galactosamine

Daizo

Egashira

Sanada

2006

J Nutr Sci Vitaminol

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SummaryThe effects of dietary corn bran hemicellulose (CBH) and neomycin (Neo) on hepatic caspase-3 activity and glycoprotein concentration were investigated to explore the possible mechanism of the alleviative action of dietary CBH and Neo on the development of D -galactosamine (GalN)-hepatitis. Rats were fed a diet containing 5% CBH with or without neomycin (Neo) for 7 or 14 d. On the last day of feeding, the rats were treated with GalN (400 mg/kg body weight, i.p.), and their plasma transaminase activities, hepatic glycoprotein concentrations and hepatic caspase-3 activities were determined 6 or 24 h later. Although the elevations of plasma transaminase activities were suppressed by CBH or Neo 24 h after GalN-treatment, the activities were not affected by CBH or Neo at an early stage (6 h) of GalN action. At 6 h, hepatic caspase-3 activity was elevated by CBH diet alone as high as that of the GalN-injected control-diet group, and the activity was not elevated further by GalN. At the same time, both GalN-treatment and CBH feeding reduced the hepatic glycoprotein (Mw. 64,000-74,000) concentration, but Neo did not affect the caspase activity or the glycoprotein concentration. These results suggest that dietary CBH elevates hepatic caspase-3 activity and reduces hepatic glycoprotein concentration, and may imply that CBH would suppress GalN-hepatitis not at the early-or middle-step of apoptosis but at the late-step of apoptosis or necrosis, although the relation between these phenomena and the alleviative effects of CBH and Neo on GalN-induced hepatitis is yet to be clarified.

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Evaluation of oxidative stress during apoptosis and necrosis caused by d-galactosamine in rat liver

Cited by 95 publications

References 31 publications

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Effect of lycopene on oxidative stress induced duringd-galactosamine/lipopolysaccharide-sensitized liver injury in rats

Red Potato Extract Protects fromD-Galactosamine-induced Liver Injury in Rats

Effects of Dietary Corn Bran Hemicellulose and Neomycin on Hepatic Caspase-3 Activity and Glycoprotein Concentration in Rats Treated with or without D-Galactosamine

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