Paroxetine Administration Alter some Biochemical Parameters in Male Wistar Rats Over a Systemic Period of Thirty-Five Days

Paroxetine is often used to treat patients with psychotic disorders, one of the side effects of this medication is that it causes erectile dysfunction in such individuals. There is a little or no information on the effect of paroxetine on some biochemical and endothelial markers of experimental models, hence the need for this research. Biochemical and endothelial functional makers in male Wistar rats were evaluated after oral administration of paroxetine for 4, 7, 21, 28 and 35 days. Seventy-two (72) male Wistar rats were grouped into two of thirty-six rats in group A (control) which received normal saline and thirty-six rats in group B (paroxetine-treated) which received 10 mg/Kg body weight of paroxetine hydrochloride for 4, 7, 14, 21, 28, and 35days respectively. During this period, six animals from the two groups were sacrificed on days 4,7,14, 21, 28 and 35 by anaesthesia using diethyl ether, blood was collected into lithium–heparinized bottles and the tissues of interest (penile and heart) of the rats were excised and preserved in ice-cold sucrose-tris buffer. Phosphodiesterase 5, arginase, nitric oxide were evaluated from the isolated tissue homogenates while cGMP, endothelin-1, creatine kinase, lipid profile and testosterone concentrations were evaluated from the plasma. The results revealed that during pre-treatment with paroxetine, there was significant (p < 0.05) 85.19 ± 4.64 and 92.58 ± 0.57 respectively PDE 5 inhibition in the penile and cardiac homogenates of rats. Nitric oxide concentration was significantly (p> 0.05) 2.96 ± 0.27 and 4.82 ± 0.05reduced while arginase activities increased significantly (p > 0.05) 272.16 ± 5.07 and 201.93 ± 11.82 during paroxetine treatment. Same trend of results were observed with plasma endothelin-1 concentration (12.88 ± 0.78), cGMP concentration (0.14 ± 0.00) and Testosterone concentration (0.46 ± 0.03) was significantly (p > 0.05) decreased during paroxetine-treatment. However, plasma creatine kinase 463.6 ± 50.96, triacyl glycerol 58.61 ± 5.49, total cholesterol 181.55 ± 9.72 and low-density lipoprotein cholesterol 165.86 ± 9.72 were significantly (p < 0.05) increased during paroxetine-treatment. However, no significant (p > 0.05) difference was observed in the high-density lipoprotein cholesterol 8.07 ± 0.46 during administration with paroxetine. From this study, it can be concluded that paroxetine administration altered erectile and endothelial markers throughout the period of administration and as such should be prescribed to patients with caution.