Bolanle Iranloye

Antifertility effect of calcium channel blockers on male rats: association with oxidative stress

PURPOSE Calcium ions are vital in many biologic processes including a variety of enzymatic reactions, activation of excitable cells, coupling of electrical activation to cellular secretion, haemostasis, bone metabolism and sperm functions. Calcium channel blockers (CCB) appear to have a reversible anti-fertility effect on male rats which does not occur through inhibition of the pituitary-gonadal axis. While the effects of CCB on male reproductive function have been investigated, less information is available regarding other reproductive indices and the underlying mechanism in the pathogenesis of male reproductive dysfunction. Therefore, the involvement of oxidative mechanisms in the adverse manifestation induced by CCB on male reproductive functions is investigated in this study. METHODS For this purpose, lipid peroxidation; enzymatic antioxidants such as superoxide dismutase, catalase and glutathione reduced; epididymal sperm count, motility; histopathology of the testes, epididymis, seminal vesicle, prostate glands; and reproductive performance were determined. RESULTS CCB administration in rats causes significant oxidative stress in the male reproductive milieu in term of increase in malondialdehyde (MDA) level and a concomitant decrease in catalase, superoxide dismutase and reduced glutathione enzyme activities in the testes. In addition, CCB treatment significantly decreased the sperm count, sperm motility, fertility index, implantation count, and litter size in this study. CONCLUSION There is substantial evidence that CCB induces significant oxidative stress in the testes, which appears to be responsible for the adverse effects of decreased sperm count and motility ultimately leading to reduced fertility in rats.

Calcium antagonists modulate oxidative stress and acrosomal reaction in rat spermatozoa.

Introduction Calcium ions are vital in many biological processes and qualify as an almost ubiquitous intracellular second messenger. This indicates the multiplicity of the effects associated with drug actions aimed at interfering with calcium ions. To examine the cellular process involved in the induction of infertility in males by calcium antagonist (CA) even in the presence of normal semen parameters, we studied the effects of different CA namely; nifedipine, verapamil and diltiazem on oxidative balance and acrosome reaction in the sperm. Material and methods For this purpose, lipid peroxidation, antioxidants such as superoxide dismutase, catalase and reduced glutathione, and acrosomal reaction were determined in sperm samples of rats. Results Calcium antagonist causes significant oxidative stress in the epididymal sperm with increased malondialdehyde level and a concomitant decrease in antioxidant activities of catalase and superoxide dismutase. The percentage value of acrosomal-reacted sperm in the nifedipine, verapamil and diltiazem-treated rats were 41 ±2.45, 39 ±2.92 and 42 ±1.22 respectively, compared with the control group value of 86 ±2.92. Conclusions It appears CA oxidatively modify the sperm resulting in functional inhibition of acrosomal reaction. Suppression of the sperm acrosomal reaction is known to have serious adverse implications for fertilization.

Reproductive parameters and oxidative stress status of male rats fed with low and high salt diet

BACKGROUND: Deficiency of minerals and micronutrients has been reported to impair the process of spermatogenesis. Historically, salt has been used by women on their husbands to increase their libido, however, the role of salt diet on sperm parameters are yet to be ascertained. AIM: The present study was designed to determine the effect of low and high salt diet on sperm parameters, oxidative status and reproductive hormone levels of male rats. MATERIALS AND METHODS: A total of 18 rats were divided into three groups: Group I: (control) received 0.3% salt diet, Group II: low salt (received 0.14% salt diet) and Group III: high salt (received 8% salt diet). All animals were treated for 6 weeks; after which epididymal sperm parameters; oxidative stress markers (malondialdehyde, glutathione, catalase and superoxide dismutase) in the testes and epididymal tissues, as well as follicle stimulating hormone (FSH), luteinizing hormone (LH) and testosterone levels were determined. RESULTS: The results showed decreased sperm count in the low salt diet rats while increased sperm count was observed in the high salt diet treated rats. Both low salt and high salt diet fed rats exhibited increased abnormal sperm cells and increased epididymal oxidative stress when compared with their respective control. FSH and testosterone levels were increased in the high salt fed rats while LH level was decreased when compared with the control values. CONCLUSION: This study suggests that both low and high salt diet play a negative role in the fertility of male rats.

Glucometabolic effects of single and repeated exposure to forced-swimming stressor in Sprague-Dawley rats

Abstract Objectives. We aimed to evaluate the effects of a single (acute) and repeated (chronic) exposure to forced-swimming stressor on glucose tolerance, insulin sensitivity, lipid profile and glycogen content in male rats. Methods. Thirty adult male Sprague-Dawley rats (12 weeks old) were divided randomly into five groups: control group, single exposure (SE) to forced-swim stressor, repeated exposure to forced-swim stressor for 7 days (RE7), 14 days (RE14) and 28 days (RE28). Glucose tolerance test and Homeostatic Model Assessment-Insulin Resistance (HOMA-IR) were undertaken on fasting rats to obtain glucose and insulin profiles. ELISA was performed to assess plasma insulin and corticosterone levels. Total cholesterol, triglyceride, high- and low-density lipoproteins, hepatic and skeletal glycogen content were also determined. Results. Repeated exposure to stressor induced glucose intolerance and insulin resistance in the experimental rats. Results showed that all RE groups exhibited a significantly higher area under the curve compared with others (p=0.0001); similarly, HOMA-IR increased (p=0.0001) in all RE groups compared with control. Prolonged exposure to stressor significantly increased the plasma insulin and corticosterone levels but decreased the glycogen content in the liver and skeletal muscle when compared with the control group. Additionally, chronic stressor significantly increased the total cholesterol and triglyceride levels, however, acute stressor produced significantly elevated high-density lipoproteins level. Conclusions. In conclusion, repeated exposure to forced-swimming stressor induced glucose intolerance and insulin resistance in rats by disrupting the insulin sensitivity as well as heightening the glycogenolysis in the liver and skeletal muscle. Acute stressor was unable to cause glucose intolerance and insulin resistance but it appears that may have a positive effect on the lipid metabolism.

Role of amygdala kisspeptin in pubertal timing in female rats

To investigate the mechanism by which maternal obesity disrupts reproductive function in offspring, we examined Kiss1 expression in the hypothalamic arcuate (ARC) and anteroventral periventricular (AVPV) nuclei, and posterodorsal medial amygdala (MePD) of pre-pubertal and young adult offspring. Sprague-Dawley rats were fed either a standard or energy-dense diet for six weeks prior to mating and throughout pregnancy and lactation. Male and female offspring were weaned onto normal diet on postnatal day (pnd) 21. Brains were collected on pnd 30 or 100 for qRT-PCR to determine Kiss1 mRNA levels. Maternal obesity increased Kiss1 mRNA expression in the MePD of pre-pubertal male and female offspring, whereas Kiss1 expression was not affected in the ARC or AVPV at this age. Maternal obesity reduced Kiss1 expression in all three brain regions of 3 month old female offspring, but only in MePD of males. The role of MePD kisspeptin on puberty, estrous cyclicity and preovulatory LH surges was assessed directly in a separate group of post-weanling and young adult female rats exposed to a normal diet throughout their life course. Bilateral intra-MePD cannulae connected to osmotic mini-pumps for delivery of kisspeptin receptor antagonist (Peptide 234 for 14 days) were chronically implanted on pnd 21 or 100. Antagonism of MePD kisspeptin delayed puberty onset, disrupted estrous cyclicity and reduced the incidence of LH surges. These data show that the MePD plays a key role in pubertal timing and ovulation and that maternal obesity may act via amygdala kisspeptin signaling to influence reproductive function in the offspring.