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This study aimed to investigate the effect of pentoxifylline on complications of prolonged usage of morphine upon the testis and sperm parameters of rats. In this study, forty male Wistar rats were divided into five groups (n = 8) and treated for 56 days to only saline, only morphine, only pentoxifylline, pentoxifylline + morphine and naltrexone + morphine. The diameters of seminiferous tubules, the maturity of germ line epithelium and sperm parameters were evaluated. The expression of inflammatory-related factors in testis tissues were also investigated at gene and protein levels. The data were calculated by one-way ANOVA test followed by Tukey's post hoc test using SPSS software for windows (version 20). Seminiferous tubule diameter, the maturity of spermatogonia and sperm parameters were significantly decreased in morphine group in comparison with control, pentoxifylline and pentoxifylline + morphine groups (p < .001). The expression of anti-inflammatory markers, at both gene and protein levels, was significantly increased in testis of morphine-treated rats in comparison with other groups (p < .001). Chronic morphine administration induces destructive effects on male reproductive system by regulating inflammatory responses. Pentoxifylline recovers the destructive effects of morphine on male reproductive system by inhibiting TLR (Toll-like receptor) activity, as an anti-inflammatory response.

Objective: Obesity is associated with reproductive disorders. Arsenic disrupts male reproduction by direct effects on the male gonads or androgens secretion. So, the present study was conducted to evaluate the toxic effects of chronic concomitant administration of high-fat diet (HF) and arsenic on the reproductive system of the male mouse. Materials and methods: In this experimental study, 72 adult male mice were randomly divided into 6 groups: low-fat diet (LF0), LF+arsenic 25 ppm, LF+arsenic 50ppm, HF0, HF+arsenic 25 ppm and, HF+arsenic 50 ppm. 24 hours after the last experimental day, plasma samples, the cauda of epididymis and testis were prepared and removed for hormonal, sperm count and histopathological assessments. Results: Testis weight and volume increased in HF0 than other groups except for LF0. Plasma LH and testosterone levels decreased in LF50, HF0, HF25, and HF50 compared to LF0. A similar effect was observed in plasma FSH levels of HF0, HF25 and HF50 groups compared with LF0. Plasma level of estradiol increased in LF50 versus to other groups. Testosterone to estradiol ratio and sperm count decreased in all groups compared to LF0. Reduced interstitial cells and large numbers of vacuoles were observed in germinal epithelium of HF0 group, that these changes were more intense in both concentrations of arsenic-treated mice. Conclusion: Present study indicated that chronic exposure to HF and arsenic-induced hypogonadotropic hypogonadism concomitant with sperm count reduction and testicular damage.

Diet is one of the important risk factors that could potentially affect arsenic-induced cardiotoxicity. The present study was undertaken to investigate the effect of high fat diet on arsenic-induced cardiotoxicity in mice. Mice were divided into six different groups (n = 12), two control groups received either low fat diet (LFD) or high fat diet (HFD) along with deionized drinking water and four test groups given LFD + 25 ppm arsenic, LFD + 50 ppm arsenic, HFD + 25 ppm arsenic, and HFD + 50 ppm arsenic in drinking water for 5 months. The body weight, heart weight to body weight ratio, cardiac biochemical markers, lipid profile, and histological examination of heart were evaluated. The results demonstrated that arsenic exposure led to a significant decrease in heart glutathione level, catalase enzyme activity, and a significant increase in reactive oxygen species (ROS), malondialdehyde levels, and biochemical enzymes. The administration of HFD resulted in above-mentioned changes as well as an alteration in lipid profile; however, arsenic exposure alone or along with HFD caused a reduction in lipid profile factors, except HDL level. Our results revealed that HFD increased arsenic-induced heart injury in the mice. This effect may be because of reduction in antioxidant activities and/or increase in oxidative stress and ROS in mice heart tissues. These findings could be important for clinical intervention to protect against or prevent arsenic-induced cardiotoxicity in humans.