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Acute exposure to cyclosporine does not increase plasma homocysteine in rats
S K Austen1, L A Fletcher, R G Fassett
1School of Human Movement Studies, University of Queensland, St Luica, Australia.
Insights
Cyclosporine A (CsA) does not increase homocysteine levels in rats, despite concerns that it may contribute to cardiovascular disease risk in transplant patients. This study found no significant effect of CsA on homocysteine concentrations.
Area of Science:
- Pharmacology
- Nephrology
- Cardiovascular Science
Background:
- Hyperhomocysteinemia is an independent risk factor for cardiovascular disease (CVD).
- Elevated homocysteine levels are observed in organ transplant recipients.
- Cyclosporine A (CsA) is a potential contributor to hyperhomocysteinemia in this population.
Purpose of the Study:
- To investigate the effect of CsA administration on plasma homocysteine levels.
- To determine if CsA influences homocysteine concentrations in a rat model.
Main Methods:
- Eighteen female Sprague Dawley rats were divided into treatment (CsA) and control (vehicle) groups.
- Rats received CsA (25 mg/kg/d) or vehicle for 18 days.
- Plasma levels of CsA, total homocysteine, and creatinine were measured post-sacrifice.
Main Results:
- No significant difference in plasma homocysteine levels was found between the CsA treatment group and the control group.
- Plasma homocysteine did not correlate with CsA concentrations.
- A positive correlation was observed between plasma homocysteine and creatinine in the CsA-treated group.
Conclusions:
- Cyclosporine A does not appear to influence plasma homocysteine concentrations in rats.
- The study suggests CsA is not a direct cause of hyperhomocysteinemia in this model.
- Further research may be needed to explore the relationship between CsA, creatinine, and homocysteine in specific contexts.
Abstract:
There is interest in the postulate that cyclosporine a (CsA) contributes to the elevated homocysteine levels seen in organ transplant recipients, as hyperhomocysteinemia is now considered an independent risk factor for cardiovascular disease (CVD) and may partially explain the increased prevalence of CVD in this population. The main purpose of this investigation was to determine the effect of CsA administration on plasma homocysteine. Eighteen female Sprague Dawley rats (4 months old) were randomly assigned to either a treatment or a control group. For 18 days the treatment group received of CsA (25 mg/kg/d) while the control group received the same volume of the vehicle. Blood samples obtained following sacrifice to measure CsA, total homocysteine, and plasma creatinine. There were no significant differences in plasma homocysteine (mean values +/- SD: treatment = 4.79 +/- 0.63 micromol/L, control = 4.46 +/- 0.75 micromol/L; P = .37). Homocysteine was not significantly correlated with final CsA concentrations (r = .17; P = .69). There was a significant difference in plasma creatinine values between the two groups (treatment = 60.44 +/- 7.68 micromol/L, control = 46.33 +/- 1.66 micromol/L; P < .001). Furthermore, plasma homocysteine and creatinine were positively correlated with the treatment group (r = .73; P < .05) but not the controls (r = -.10; P = .81). In conclusion, CsA does not influence plasma homocysteine concentrations in rats.