Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:2.6.1.2 (
alanine aminotransferase
)
26,722
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The involvement of non-enzymatic antioxidant defenses in the protective effect of diphenyl diselenide (PhSe)(2) on testicular damage caused by cadmium in mice was investigated. Mice received a single dose of CdCl(2) (5mg/kg, intraperitoneally). Thirty minutes after the CdCl(2) injection, they received a single oral dose of (PhSe)(2) (400micromol/kg). Twenty-four hours after CdCl(2) administration, blood samples were collected and mice were killed and had their testes dissected. Parameters in plasma (aspartate (AST) and alanine (
ALT
) aminotransferases and lactato dehydrogenase (LDH) activities as well as creatinine levels) were determined. The activity of
delta-aminolevulinate dehydratase
(delta-ALA-D), the levels of thiobarbituric acid-reactive substances (TBARS), ascorbic acid and nonprotein thiols (NPSH) and histological analysis were determined in collected samples. Results demonstrated that (PhSe)(2) protected against toxicity induced by CdCl(2) on delta-ALA-D activity, ascorbic acid and NPSH levels. (PhSe)(2) protected against the increase in plasma AST,
ALT
and LDH activities caused by CdCl(2). Testes of mice exposed to CdCl(2) showed marked histopathological alterations that were ameliorated by administration of (PhSe)(2). (PhSe)(2) protected against toxicity induced by CdCl(2) in testes of mice. Ascorbic acid and NPSH, non-enzymatic antioxidant defenses, are involved in the protective effect of (PhSe)(2) against testicular damage caused by CdCl(2) in mice.
...
PMID:Involvement of non-enzymatic antioxidant defenses in the protective effect of diphenyl diselenide on testicular damage induced by cadmium in mice. 1974 28
Strategies to diminish cadmium (Cd) absorption are highly desirable especially where Cd exposure due to environmental contamination is still inevitable. Cd toxicity may be influenced by dietary components, such as fiber and minerals. Multimixtures are low-cost cereal bran supplements used in Brazil and in other countries to counteract malnutrition in low-income populations. This study was aimed at evaluating whether multimixture would reduce Cd effects in young rats. Animals received a diet with or without the multimixture plus 0, 5, or 25 mg Cd/kg (control, Cd-5, and Cd-25 groups) during 30 days. The Cd-5 groups were similar to control groups in all parameters analyzed, except in the higher renal Cd concentration. However, the Cd-25 groups had lower biological growth parameters and renal
delta-aminolevulinate dehydratase
activity, besides higher renal Cd concentration and plasma
alanine aminotransferase
activity compared to the controls. The multimixture did not prevent Cd effects in the Cd-25 group, but caused a small reduction in renal Cd concentration in the Cd-5 group. Although this multimixture was ineffective to prevent Cd effects at the higher concentration, it seemed to reduce Cd accumulation at the lower Cd dietary concentration, which is similar to levels of human exposure in some polluted areas.
...
PMID:Influence of cereal bran supplement on cadmium effects in growing rats. 2001 94
Organoselenides have been documented as promising pharmacological agents against a number of diseases associated with oxidative stress. Here we have investigated, for the first time, the potential antioxidant activity of binaphthyl diselenide ((NapSe)(2); 50 mg kg(-1), p.o.) against the 2-nitropropane (2-NP)-induced hepatoxicity in rats, using different end points of toxicity (liver histopathology, plasma aspartate aminotransferase (AST),
alanine aminotransferase
(
ALT
) and creatinine). In addition, in view of the association of oxidative stress with 2-NP exposure, hepatic lipid peroxidation, ascorbic acid levels,
delta-aminolevulinate dehydratase
(delta-ALA-D) and catalase (CAT) activities were evaluated. 2-NP caused an increase of AST,
ALT
and hepatic lipid peroxidation. 2-NP also caused hepatic histopathological alterations and delta-ALA-D inhibition. (NapSe)(2) (50 mg kg(-1)) prevented 2-NP-induced changes in plasmatic
ALT
and AST activities and also prevented changes in hepatic histology, delta-ALA-D and lipid peroxidation. Results presented here indicate that the protective mechanism of (NapSe)(2) against 2-NP hepatotoxicity is possibly linked to its antioxidant activity.
...
PMID:Protective effect of binaphthyl diselenide, a synthetic organoselenium compound, on 2-nitropropane-induced hepatotoxicity in rats. 2051 88
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