ABSTRACT
Buchholzia coriacea has been reported to possess antifertility activities but little is known of the mechanisms responsible. This study was therefore designed to examine the mechanism responsible for the action of Buchholzia coriacea. Eighteen male Wistar rats (180-200 g) were used for this study. They were grouped into 3 (n = 6) namely, Control, Methanolic fraction of Buchholzia coriacea (MFBC) 50 mg/kg, and MFBC 100 mg/kg administered orally with respective dosage. After 6 weeks of administration, rats were euthanized, serum collected, while testes, epididymis and prostate were excised and homogenized. Testicular protein and testosterone, aromatase and 5α-reductase enzyme, 3ß hydroxysteroid dehydrogenase (HSD), 17ß-HSD, interleukin (IL) 1ß, IL-10 and Prostatic specific enzyme antigen (PSA) were assessed and data analyzed with ANOVA. There were significant increases in 3ß-HSD and 17ß-HSD levels in the MFBC 50 mg/kg with corresponding decreases in MFBC 100 mg/kg when compared to control. IL-1 was decreased in both doses while IL-10 increased in both doses compared to control. 5-α reductase enzyme was significantly decreased in the MFBC 100 mg/kg relative to the control. Testicular protein, testosterone and aromatase enzyme were not significantly different at both doses compared to control. PSA was significantly increased in the MFBC 100 mg/kg but not the 50 mg/kg relative to control. MFBC exhibits antifertility properties by interfering with testicular enzymes and inflammatory cytokines.
Subject(s)
Aromatase , Testis , Humans , Rats , Male , Animals , Testis/metabolism , Aromatase/metabolism , Interleukin-10/metabolism , Cytokines/metabolism , Prostate-Specific Antigen/metabolism , Rats, Wistar , TestosteroneABSTRACT
The negative influence of cigarette smoking on developing fetus is well documented but reports of prenatal cigarette smoking on male reproductive hormones are controversial. However, shortened anogenital distance (AGD) has been established to be an indicator of potential male infertility. We therefore investigated the effects of prenatal exposure to passive cigarette smoke on AGD, reproductive hormones and oxidative stress biomarkers of Wistar rats. Female rats were randomly divided into two groups (n=5) and cohabited with male. Group 1 was exposed to smoke from an idling cigarette from day 1 of gestation till parturition, while Group 2 served as control (no-exposure). Morphometric variables of the litters were recorded on postnatal day 1 (PND1) and at 6th week postnatal life. The male offspring were then sacrificed by cervical dislocation. Testosterone, luteinizing hormone (LH) and follicle stimulating hormone (FSH) were analysed using ELISA. Serum levels of Catalase, sodium dismutase (SOD), malondialdehyde (MDA), lipid profile and liver function biomarkers were examined spectrophotometrically. On PND1, crown rump length and total body length of rats prenatally exposed to cigarette smoke were significantly shorter. Significantly shorter AGD and crown rump length were also observed at 6th week. Testosterone, LH and FSH were not significantly affected. Cigarette smoke exposure significantly decreased Catalase and SOD while MDA increased. Liver function biomarkers, HDL and LDL were not affected but serum levels of total cholesterol and triglyceride significantly increased. The observed decline in AGD and precipitation of oxidative stress by intrauterine cigarette smoke exposure may predispose to male infertility at adulthood.