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Possible effects of interferon-alpha on Fas-induced renal apoptosis in mouse
T Cvetkovic1, G Kocic, T Jevtovic-Stoimenov
1Institute of Biochemistry, Medical Faculty, University of Nis, Serbia. tanja_cvetkovic@yahoo.co.uk
Unlabelled:
Fas (APO-1/CD95) is a cell surface receptor that initiates apoptotic pathway. Fas-stimulated ROS generation may play important role in Fas-mediated apoptosis. The aim of this study was to evaluate the influence of interferon-alpha on oxidative stress parameters in Fas-induced renal apoptosis in mice kidney.
Subjects And Methods:
One-month-old Balb C male mice were used for the study. The animals were divided in four groups: group 1 were the controls, group 2 mice were treated with anti-Fas antibody i.p., group 3 mice were treated with IFN-alpha, and group 4 mice were treated with both agents simultaneously. The mice were killed 48 h afterwards, and kidneys were homogenized. TBA reactive substances (TBARS), glutathione content, and reactive carbonyl group (RCG) were measured.
Results:
The results showed a statistically significant increase of TBARS (p < 0.05) and RCG (p < 0.05) concentration in the group treated with anti-Fas antibody versus control. IFN-alpha decreased the concentration of TBARS and RCG after anti-Fas antibody administration (p < 0.05). There is no significant difference in glutathione content between investigated groups.
Conclusion:
IFN-alpha might be considered as a new target for therapeutic intervention in FasL/Fas induced renal injury.
Insights
Interferon-alpha (IFN-alpha) reduces oxidative stress in mice kidneys following Fas-induced apoptosis. This suggests IFN-alpha may protect against FasL/Fas induced renal injury.
Area of Science:
- Immunology
- Nephrology
- Cell Biology
Background:
- Fas receptor (APO-1/CD95) triggers apoptosis.
- Fas-stimulated reactive oxygen species (ROS) generation is implicated in Fas-mediated apoptosis.
- Investigating oxidative stress in Fas-induced renal apoptosis is crucial.
Purpose of the Study:
- To evaluate the effect of interferon-alpha (IFN-alpha) on oxidative stress markers.
- To assess IFN-alpha's role in Fas-induced renal apoptosis in mice.
Main Methods:
- Balb C mice were divided into four groups: control, anti-Fas antibody, IFN-alpha, and combination treatment.
- Kidneys were analyzed for thiobarbituric acid reactive substances (TBARS), glutathione, and reactive carbonyl groups (RCG).
Main Results:
- Anti-Fas antibody significantly increased TBARS and RCG levels.
- IFN-alpha administration reduced TBARS and RCG levels post anti-Fas antibody treatment.
- Glutathione content showed no significant differences between groups.
Conclusions:
- IFN-alpha demonstrates a protective effect against oxidative stress in Fas-induced renal injury.
- IFN-alpha may serve as a therapeutic target for FasL/Fas mediated kidney damage.
