Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    ISSN: 1437-7799
    Keywords: glycerol-induced acute renal failure ; glutathione ; theophylline ; buthionine sulfoximine ; heme oxygenase-1 ; oxidant stress
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Background To investigate the mechanism of glycerol-induced renal injury, we examined kidney levels of the cellular antioxidant glutathione and heme oxygenase-1 (HO-1), the rate-limiting enzyme in heme degradation, after glycerol injection. Methods Male Wistar rats were injected with glycerol to induce acute renal failure. Serum creatinine levels were used as a marker of renal function at 24 hours after glycerol injection. Theophylline and buthionine sulfoximine or vehicle were administered to the rats after glycerol injection, and we determined renal glutathione levels (by biochemical assay) and the levels of HO-1 protein and messenger ribonucleic acid (mRNA; using immunoblot analysis [kidney only]) in various rat organs at 24 hours after glycerol injection. Results Glutathione levels abruptly declined after glycerol injection, reached a minimum at 4 hours, then returned to about two thirds of control levels at 24 hours. HO-1 protein was detected at 4 hours and reached a maximum at 24 hours. The induction of HO-1 protein was observed only in the kidney. HO-1 mRNA was faintly expressed at 2 hours, increased until at least 8 hours, and was not detected 24 hours after the treatment. When theophylline was administered to glycerol-injected rats, renal function improved and glutathione levels increased. In addition, the levels of HO-1 protein decreased, compared with those of glycerol-treated rats not given theophylline. Conclusions These results suggest that theophylline may act by modulating the HO-1 directly or indirectly.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    ISSN: 1436-2813
    Keywords: Key Words: methionine adenosyltransferase ; oxidative stress ; ischemia ; reperfusion ; liver
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: 10 (CoQ10) was administered to rats prior to ischemia, both the reduction in the MAT activity and hepatic GSH levels induced by ischemia–reperfusion were protected. Our findings suggest that CoQ10 may posttranslationally regulate the MAT activity via the changes in the GSH level in the liver.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1432-1912
    Keywords: Key words 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone ; O6-methylguanine ; K-ras mutation ; Vitamin E ; Lung tumorigenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to estimate the effect of vitamin E on DNA injury and K-ras point mutation at an early stage of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK)-induced lung tumorigenesis in mice, the present study was carried out. Presupplement with vitamin E about 15 times more than control for a week significantly inhibited NNK-induced O6-methylguanine formation in the lungs of mice at 4 and 168 h after the injection. At 30 days after the NNK injection, the activation of K-ras oncogene with a 12th codon GC→AT transition was detected in 56% of lung samples tested by mutant-allele-specific amplification. Vitamin E supplement reduced the frequency of the mutation to 30%. These results suggest that vitamin E suppresses NNK-induced DNA injury and subsequent fixation of the injury during the initiation and post-initiation phases of the lung tumorigenesis in mice.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...