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Jamba, L.; Nehru, Bimla; Bansal, M. P.

doi:10.1023/a:1006869623864

Cited by 33 publications

(11 citation statements)

References 26 publications

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“…Therefore we used an M r value of 55 kDa per FAD‐containing TrxR subunit for stoichiometric calculations. With respect to the selenium content, thioredoxin reductase represents one and possibly the only function associated with the 55–60 kDa band described for mouse selenoprotein maps [6, 7].…”

Section: Resultsmentioning

confidence: 99%

The 58 kDa mouse selenoprotein is a BCNU‐sensitive thioredoxin reductase

1997

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Section: Resultsmentioning

confidence: 99%

The 58 kDa mouse selenoprotein is a BCNU‐sensitive thioredoxin reductase

1997

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“…Further, it has been shown that pretreatment with catalase [48] superoxide dismutase [49] or S-adenosylmethionine [50] prevents APAPinduced liver necrosis. Moreover, both thioredoxin and protein disulfide isomerase regulate oxidation/reduction of proteins and share a common motif (cys-X-X-cys) with acetaminophen-binding protein [51]. The observed changes in protein levels were largest for the high dose of APAP and moderate for the low dose.…”

Section: Discussionmentioning

confidence: 99%

Two-dimensional database of mouse liver proteins: Changes in hepatic protein levels following treatment with acetaminophen or its nontoxic regioisomer 3-acetamidophenol

et al. 2000

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Overdose of acetaminophen (APAP) causes acute hepatotoxicity in rodents and man. The mechanism underlying APAP-induced liver injury remains unclear, but experimental evidence strongly suggests that activation of APAP and subsequent formation of protein adducts are involved in hepatotoxicity. Using proteomics technologies, we constructed a two-dimensional protein database for mouse liver, comprising 256 different gene products and investigated the proteins affected after APAP-induced hepatotoxicity. Adult male mice received a single dose of APAP (100 or 300 mg/kg) or its nontoxic regioisomer 3-acetamidophenol (AMAP, 300 mg/kg). The extent of liver damage was assessed 8 h after administration by increased liver enzyme release and histopathology. Changes in the protein level were studied by comparison of the intensities of the corresponding spots on two-dimensional (2-D) gels. The expression level of about 35 of the identified proteins was modified due to treatment with APAP or AMAP. The observed changes were usually in the order of 10-50% of the control value and were more marked in the high- than in the low-dose of APAP-treated animals. Most of the changes caused by AMAP occurred in a subset of the proteins modified by APAP. Many of the proteins showing changed expression levels are either known targets for covalent modification by N-acetyl-p-benzoquinoneimine (NAPQI) or involved in the regulation of mechanisms that are believed to drive APAP-induced hepatotoxicity.

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“…The groupings were as follows: group A (control) received 0.5 ml of distilled water, group B received 8 mg/kg body weight (b.w.) of Cd,[2] group C, 8 mg/kg b.w. of Cd and 100 mg/kg b.w.…”

Section: Methodsmentioning

confidence: 99%

“…[1] Cadmium is capable of inducing irreparable damage to vital organs of the animals such as the liver and kidney during acute and chronic exposures. [2] It is also widely accepted that Cd causes tissue damage by membrane lipid peroxidation because of its ability to generate free radicals and inhibit or reduce the activity of antioxidant enzymes like glutathione peroxidase, glutathione reductase, catalase, and superoxide dismutase (SOD). [2] Cadmium and oxidative stress seem to be related, as the production of oxygen free radicals responsible for its toxicity has been found to be stimulated in Cd -treated rats.…”

Section: Introductionmentioning

confidence: 99%

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In vitro and in vivo antioxidant activities of the aqueous extract of Celosia argentea leaves

2011

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Objective:The aqueous extract of Celosia argentea var. cristata L. leaves at 100, 200, and 400 mg/kg body weight (b.w.) was investigated against cadmium (Cd)-induced oxidative stress in Wistar rats. The in vitro antioxidant of the extract was evaluated using ammonium thiocyanate, reducing power, and membrane stabilizing models.Materials and Methods:For the in vivo study, 30 male rats (Rattus norvegicus) weighing 138.02 ± 7.02 g were completely randomized into 6 groups (A–F) of 5 animals each. Animals in groups A and B received 0.5 ml of distilled water and the same volume containing 8 mg/kg b.w. of Cd, respectively, for 7 days orally. Animals in groups C, D, E, and F were treated like those in group B except that they received 100 mg/kg b.w. of ascorbic acid, and 100, 200, and 400 mg/kg b.w. of the extract, respectively, in addition to Cd.Results:Phytochemical screening revealed the presence of alkaloids (0.61%), saponins (2.93%), cardiac glycosides (0.21%), cardenolides (0.20%), phenolics (3.26%), and flavonoids (2.38%). A total of 10 mg/ml of the extract inhibited linoleic acid oxidation by 67.57%. The highest reducing power was 100 mg/ml as against 10 mg/ml for ascorbic acid. In addition, 2 mg/ml of the extract produced a membrane stabilizing activity of 63.49% as against 77.46% for indomethacin. Compared with the distilled water control group, the administration of Cd alone significantly (P < 0.05) decreased the alkaline phosphatase activity of the rat liver and brain. This decrease was accompanied by a corresponding increase in the serum enzyme. The simultaneous administration of the extract and Cd produced an enzyme activity that compared favorably (P > 0.05) with the animals that received Cd and ascorbic acid. In addition, the reduction in the superoxide dismutase and catalase activity of the liver and brain of the animals, serum uric acid, albumin and bilirubin, and also the increase in the serum malondialdehyde content in animals treated with Cd alone was attenuated by the extract; the values compared well (P > 0.05) with those simultaneously administered with Cd and ascorbic acid.Conclusion:Overall, the results indicated that the aqueous extract of C. argentea leaves attenuated Cd-induced oxidative stress in the animals, with the best result at 400 mg/kg b.w. The antioxidant activity of the extract may be attributed to the phenolic and flavonoid components of the extract. The induction of antioxidant enzymes and scavenging of free radicals may account for the mechanism of action of the extract as an antioxidant.

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Untitled

Cited by 33 publications

References 26 publications

The 58 kDa mouse selenoprotein is a BCNU‐sensitive thioredoxin reductase

The 58 kDa mouse selenoprotein is a BCNU‐sensitive thioredoxin reductase

Two-dimensional database of mouse liver proteins: Changes in hepatic protein levels following treatment with acetaminophen or its nontoxic regioisomer 3-acetamidophenol

In vitro and in vivo antioxidant activities of the aqueous extract of Celosia argentea leaves

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