Introduction Premature ejaculation (PE) is the most common male sexual dysfunction with many lines of treatment that show conflicting results. Paroxetine and tramadol were both reported to be effective in treatment of PE. Aim To investigate the effectiveness of long-term daily paroxetine vs. on-demand tramadol HCl in treatment of PE. Main Outcome Measures Intravaginal ejaculatory latency time (IELT) and Arabic Index of PE (AIPE) were used to assess the efficacy of investigated drugs. Methods Thirty-five cases with lifelong PE were enrolled in this study. Baseline recording of IELT using a stop watch and AIPE was done. Patients were randomized to take tramadol HCl on-demand or daily paroxetine. Reassessment was done after 6 and 12 weeks. A wash-out period for 2 weeks was given before cross-over to the other medication. Assessment of the effect of the second medication after 6 and 12 weeks was done. Results Tramadol and paroxetine increased IELT significantly after 6 weeks by seven- and 11-folds, respectively, compared with baseline. After 12 weeks, a decline of IELT to fivefolds was recorded with tramadol whereas further increase of IELT to 22-folds was recorded with paroxetine compared with baseline (P <0.05). Tramadol improved AIPE score significantly after 6 weeks but not after 12 weeks vs. baseline, whereas paroxetine increased the AIPE score after 6 and 12 weeks vs. baseline (P <0.05). Conclusions Daily paroxetine is more effective than on-demand tramadol for treatment of lifelong PE. Tramadol is not recommended as a long-term treatment of lifelong PE.

Oxidative stress has been implicated in reproductive toxicity induced by antipsychotics (APs). This study aims to further investigate the role of AP-induced oxidative stress in reproductive dysfunction. Thirty adult female albino rats were divided into three groups including a control group (n = 10) receiving distilled water, HAL group (n = 10) receiving haloperidol (HAL) (2 mg/kg/day), and CLZ group (n = 10) receiving clozapine (CLZ) (20 mg/kg/day). After 28 days, the rats were anesthetized, blood was withdrawn from their hearts, and ovaries were removed before they were sacrificed. Serum prolactin concentrations were measured. For each rat, one ovary was used for biochemical studies including mitochondrial complexes I and III activities and oxidative stress markers (lipid peroxidation, super oxide dismutase [SOD], catalase [CAT], and reduced glutathione [GSH]). The other ovary was used for histopathological examination and immunohistochemistry staining for p53 and Ki-67. HAL-treated rats showed significantly (p < 0.001) higher serum prolactin concentrations compared with other groups. HAL significantly inhibited complexes I (p < 0.001) and III activities (p < 0.05), while CLZ inhibited only complex I (p < 0.001). Lipid peroxidation was increased by HAL (p < 0.001) and CLZ (p < 0.01). HAL caused significant (p < 0.001) reductions in SOD, CAT, and GSH. CLZ caused a significant decrease in SOD (p < 0.001) and GSH (p < 0.01) with no effect on CAT. Histopathological studies of CLZ-and HAL-treated ovaries showed features suggestive of hyperprolactinemia and oxidative stress. Ki-67-and P53-immunostained sections were suggestive of disruption of cellular proliferation. These findings support the hypothesis that HAL and CLZ induce reproductive dysfunction through mechanisms involving ovarian mitochondrial dysfunction and oxidative stress.

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