Displaying publications 21 - 24 of 24 in total

Abstract:
Sort:
  1. Boettiger DC, Saphonn V, Lee MP, Phanuphak P, Pham TT, Heng Sim BL, et al.
    J Acquir Immune Defic Syndr, 2014 Dec 01;67(4):e131-3.
    PMID: 25197829 DOI: 10.1097/QAI.0000000000000338
    Matched MeSH terms: Kidney Diseases/chemically induced*
  2. Ansar S, Iqbal M, AlJameil N
    Hum Exp Toxicol, 2014 Dec;33(12):1209-16.
    PMID: 24596035 DOI: 10.1177/0960327114524237
    Ferric nitrilotriacetate (Fe-NTA) induces tissue necrosis as a result of lipid peroxidation (LPO) and oxidative damage that leads to high incidence of renal carcinomas. The present study was undertaken to evaluate the effect of diallyl sulphide (DAS) against Fe-NTA-induced nephrotoxicity. A total of 30 healthy male rats were randomly divided into 5 groups of 6 rats each: (1) control, (2) DAS (200 mg kg(-1)), (3) Fe-NTA (9 g Fe kg(-1)), (4) DAS (100 mg kg(-1)) + Fe-NTA (9 mg Fe kg(-1)) and (5) DAS (200 mg kg(-1)) + Fe-NTA (9 mg Fe kg(-1)). Fe-NTA + DAS-treated groups were given DAS for a period of 1 week before Fe-NTA administration. The intraperitoneal administration of Fe-NTA enhanced blood urea nitrogen and creatinine levels with reduction in levels of antioxidant enzymes. However, significant restoration of depleted renal glutathione and its dependent enzymes (glutathione reductase and glutathione-S-transferase) was observed in DAS pretreated groups. DAS also attenuated Fe-NTA-induced increase in LPO, hydrogen peroxide generation and protein carbonyl formation (p < 0.05). The results indicate that DAS may be beneficial in ameliorating the Fe-NTA-induced renal oxidative damage in rats.
    Matched MeSH terms: Kidney Diseases/chemically induced
  3. Alharazy SM, Kong N, Saidin R, Gafor AH, Maskon O, Mohd M, et al.
    Angiology, 2014 Mar;65(3):225-6.
    PMID: 23564021 DOI: 10.1177/0003319713483544
    Matched MeSH terms: Kidney Diseases/chemically induced*
  4. Abdulla MH, Sattar MA, Johns EJ, Abdullah NA, Khan MA
    Eur J Nutr, 2011 Dec;50(8):689-97.
    PMID: 21373947 DOI: 10.1007/s00394-011-0180-9
    AIM: To explore the hypothesis that high fructose intake results in a higher functional contribution of α1A-adrenoceptors and blunts the adrenergically and angiotensin II (Ang II)-induced renal vasoconstriction.

    METHODS: Twelve Sprague-Dawley rats received either 20% fructose solution [FFR] or tap water [C] to drink ad libitum for 8 weeks. The renal vasoconstrictor response to noradrenaline (NA), phenylephrine (PE), methoxamine (ME) and Ang II was determined in the presence and absence of 5-methylurapidil (5-MU) (α1A-adrenoceptor antagonist) in a three-phase experiment (pre-drug, low- and high-dose 5-MU). Data, mean ± SEM were analysed by ANOVA or Student's unpaired t-test with significance at P < 0.05.

    RESULTS: FFR exhibited insulin resistance (HOMA index), hypertension and significant increases in plasma levels of glucose and insulin. All agonists caused dose-related reductions in cortical blood perfusion that were larger in C than in FFR while the magnitudes of the responses were progressively reduced with increasing doses of 5-MU in both C and FFR. The degree of 5-MU attenuation of the renal cortical vasoconstriction due to NA, ME and Ang II was significantly greater in the FFR compared to C.

    CONCLUSIONS: Fructose intake for 8 weeks results in smaller vascular response to adrenergic agonists and Ang II. The α1A-adrenoceptor subtype is the functional subtype that mediates renal cortical vasoconstriction in control rats, and this contribution becomes higher due to fructose feeding.

    Matched MeSH terms: Kidney Diseases/chemically induced
Filters
Contact Us

Please provide feedback to Administrator (afdal@afpm.org.my)

External Links