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Published on: December 4, 2007
Pathophysiology of sildenafil-induced ocular toxicity in rats and treatment
Ibrahim Cicek1, Busra Caliskan2, Bulent Yavuzer3
1Department of Ophthalmology, Faculty of Medicine, Erzincan Binali Yıldırım University, Erzincan 24100, Türkiye.
Aim:
To examine the ocular toxicity linked to sildenafil usage and the possible protective benefits of adenosine triphosphate (ATP) against this toxicity in rats.
Methods:
Twenty-four male albino Wistar-type rats were divided into four equal groups (n=6/group) as follows: healthy group (HG), ATP-only group (ATPG), sildenafil-only group (SILG), and ATP+sildenafil group (ATP+SLD). ATPG and ATP+SLD groups were injected intraperitoneally with ATP (4 mg/kg), while SILG and HG groups were injected with saline (0.9% NaCl) by the same route as a solvent. One hour after the administration of ATP and solvent, sildenafil (10 mg/kg) was administered orally to the SILG and ATP+SLD groups. This procedure was repeated once a day for 4wk. The animals were then sacrificed, eyeballs were removed and oxidant and antioxidant parameters were measured biochemically. Additionally, the ocular tissues were evaluated histopathologically.
Results:
Sildenafil increased oxidant (malondialdehyde) levels and decreased antioxidant levels (total glutathione, superoxide dismutase, catalase) in rat ocular tissues and caused severe oxidative stress. In addition, sildenafil has been shown histopathologically to cause oxidative damage in retinal layers. ATP treatment suppressed oxidative stress and attenuated histopathological damage in the retinal layers.
Conclusion:
ATP protects retinal tissue against sildenafil-induced ocular oxidative damage in rats and may contribute to the development of novel approaches to prevent or treat this damage.
Insights
Adenosine triphosphate (ATP) protects rat eyes from sildenafil-induced oxidative damage. This study shows ATP can mitigate sildenafil
Area of Science:
- Ocular toxicology
- Biochemistry
- Pharmacology
Background:
- Sildenafil, a common erectile dysfunction drug, may cause ocular toxicity.
- Oxidative stress is implicated in sildenafil-induced eye damage.
- Adenosine triphosphate (ATP) is investigated for potential protective effects.
Purpose of the Study:
- To investigate the ocular toxicity of sildenafil in rats.
- To evaluate the protective role of adenosine triphosphate (ATP) against sildenafil-induced ocular toxicity.
Main Methods:
- Rats were divided into four groups: control, ATP-only, sildenafil-only, and ATP+sildenafil.
- Animals received daily intraperitoneal ATP or saline, followed by oral sildenafil or saline for 4 weeks.
- Ocular tissues were analyzed for oxidant/antioxidant parameters and histopathological changes.
Main Results:
- Sildenafil significantly increased oxidative stress markers (malondialdehyde) and decreased antioxidant levels (glutathione, SOD, catalase) in rat eyes.
- Histopathological examination revealed sildenafil caused retinal oxidative damage.
- ATP administration attenuated oxidative stress and reduced retinal damage caused by sildenafil.
Conclusions:
- ATP demonstrates a protective effect against sildenafil-induced ocular oxidative damage in a rat model.
- ATP may offer a therapeutic strategy to prevent or treat sildenafil-related eye toxicity.
