Moringa oleifera restored semen quality, hormonal profile, and testicular morphology against Highly Active Antiretroviral Therapy-induced toxicity in adult male Wistar rats.

OBJECTIVE: Reproductive toxicity has been greatly linked with Highly Active Antiretroviral Therapy (HAART) use. This study investigated the effects of Moringa oleifera Leaf Extract (MOE) on HAART-induced testicular toxicity in adult male Wistar rats. METHODS: Twenty adult male Wistar rats (150-200 g) were assigned into four groups (n=5). Group A received distilled water; Group B received (orally) 200 mg/kg BW HAART only; Group C received (orally) 200 mg/kg BW HAART and 100 mg/kg BW MOE (low dose group) and Group D received (orally) 200 mg/kg BW HAART and 300 mg/kg BW MOE. At the end of the 28-day experiment, body and testicular weights were measured; serum and testis obtained were subjected to hormone profiling, biochemical and histological studies. RESULTS: HAART caused a significant decrease in body and testicular weight, testicular distortion and spermatogenic cell disorganization, altered semen quality and function, hormonal profiles, and oxidative stress markers (SOD, CAT, GSH) were significantly decreased with the concurrent increase in MDA level. However, treatment with MOE improved sperm parameters, testis morphology, antioxidants markers, and hormones assessments. CONCLUSIONS: The exposure to HAART produced marked testicular toxicity, ameliorated using Moringa oleifera leaf extract, thereby preserving testicular physiological function and morphology.

Protective role of Allium cepa Linn (onion) juice on maternal dexamethasone induced alterations in reproductive functions of female offspring of Wistar rats.

Maternal treatment with dexamethasone induces oxidative stress in the reproductive structures of offspring. Consumption of Allium cepa Linn improves antioxidant status. This study was designed to evaluate the protective role of Allium cepa Linn juice on maternal dexamethasone induced alterations in reproductive functions of the female offspring of Wistar rats. Twenty lactating dams (180-200 â€‹g) were randomly assigned into four groups (n â€‹= â€‹5) on the day of parturition and treated as follows during lactation for 21 days: Control (5 â€‹ml/kg BW distilled water); Dexamethasone (60 â€‹µg/kg BW); Allium cepa (5 â€‹ml/kg BW); Dexamethasone â€‹+ â€‹Allium cepa (60 â€‹µg/kg BW â€‹+ â€‹5 â€‹ml/kg BW). The female offspring were separated at birth. Days of vaginal opening and first oestrus cycle, length and frequency of estrous cycle as well as serum hormonal profiles were assessed as measure of reproductive functions. Ovarian superoxide dismutase (SOD) activity, catalase activity and malondialdehyde (MDA) level were measured as indices of oxidative stress. Oestrous cycle length, frequencies of diestrus as well as the Ovarian MDA were significantly increased (p â€‹< â€‹0.05) in dexamethasone (DEX) group relative to control group. Serum 17ß-oestradiol and corticosterone level in addition to SOD and catalase activities were significantly reduced (p â€‹< â€‹0.05) in DEX group relative to control. Co-administration of Dex with Allium cepa Linn juice reduced the oestrous length, frequency of diestrous as well as ovarian MDA. There was also a significant increase in serum 17ß-oestradiol, ovarian SOD and catalase activity. The results suggest that Allium cepa could protect against alterations in reproductive functions of offspring induced by maternal treatment with dexamethasone during lactation in Wistar rats. The flavonoid constituent of onion may also help in reducing oxidative stress in the offspring.

Allium cepa Linn juice protect against alterations in reproductive functions induced by maternal dexamethsone treatment during lactation in male offspring of Wistar rats.

Treatment with dams with dexamethasone during lactation has been reported to induce oxidative stress in the testis of the offspring. Allium cepa L (Red Onion) is known to be a potent free radical scavenger. The protective role of Allium cepa against oxidative stress induced in testis following treatment with dexamehasone during lactation in Wistar rats was assessed. Twenty female rats were assigned into four groups (n = 5) during lactation and they were treated as follows: Group 1 serve as Control (distilled water), Group 2, 3, and four were admistered dexamethasone (60 µg/kg), Allium cepa (5 ml/kg) and dexamethasone + Allium cepa respectively. Testicular descent, pubertal age, sperm quality indices, and serum hormonal profile were assessed as indices of reproductive function. Testicular malondialdehyde (MDA) reduced glutathione (GSH) as well as superoxide dismutase (SOD) and catalase activities were assessed as measures of oxidative stress. Results obtained showed that dexamethasone caused significant (P < 0.05) reduction in testes weights, indices of sperm quality, serum testosterone, FSH, LH levels and testicular antioxidant enzyme activities. There was significant delay (P < 0.05) in days of testes descent, preputial separation and increase in testicular MDA. However, maternal treatment with Allium cepa Linn juice significantly (P < 0.05) improved both indices of reproductive function and testicular antioxidant enzymes. These findings suggest that Allium cepa Linn has a protective effect against testicular oxidative stress and reproductive dysfunction following treatment of dams with dexamethasone during lactation.

Experimental maternal treatment with dexamethasone during lactation induces neonatal testicular and epididymal oxidative stress; Implications for early postnatal exposure.

Maternal treatment with dexamethasone during lactation alters reproductive functions and increases serum corticosterone in the male offspring. Excess corticosterone may induce oxidative stress. This study was designed to evaluate the effects of maternal treatment with dexamethasone during lactation on oxidative stress indices in the testis and epididymis of a male offspring. Twenty lactating dams were divided into 4 groups (n=5). Group 1 was administered 0.02ml/100g/day normal saline subcutaneously at lactation days 1-21. Groups 2, 3, and 4 were administered 100µg/kg/day dexamethasone (Dex) subcutaneously at lactation days (LD) 1-7, 1-14, and 1-21 respectively. Testis and epididymis malondialdehyde (MDA), catalase and superoxide dismutase (SOD) activities were measured as markers of oxidative stress. The mean testis and epididymis MDA were significantly raised (p<0.05) in the dexamethasone-treated groups when compared with control. This was accompanied with a significant reduction (p<0.05) in SOD and catalase activities in these tissues in the DexLD 1-21, when compared with control. The mean total protein level of the epididymis was significantly reduced (p<0.05) in all the dexamethasone treated groups when compared with control. In conclusion, maternal treatment with dexamethasone during the first two weeks of lactation and throughout lactation may lead to increase in oxidative stress in the testis and epididymis of the male offspring of Wistar rats.

Maternal treatment with dexamethasone during gestation alters sexual development markers in the F1 and F2 male offspring of Wistar rats.

Maternal treatment with dexamethasone (Dex) in threatening preterm delivery alters activities at the hypothalamic-pituitary-adrenal axis in the offspring. This alteration may interfere with reproductive function. The impact of gestational Dex exposure on male reproductive function of the offspring was investigated. A total of 25 pregnant rats randomly assigned to five groups (n=5) were treated with normal saline (control), Dex (100 µg/kg/day sc) during gestation days (GD) 1-7, 8-14, 15-21 and 1-21, respectively. Birth weight, anogenital distance (AGD), pubertal age, sperm parameters, hormonal profile and histopathology of testis and epididymis were determined in the F1 and F2 offspring. Results showed a significant increase (P<0.05) in pubertal age, serum corticosterone and gonadotropin-releasing hormone (GnRH) levels in the male offspring of DexGD 15-21 and 1-21 groups and a significant decrease (P<0.05) in serum testosterone, luteinizing hormone, birth weight and AGD at birth in the male F1 offspring. In the F2 offspring, there was a significant reduction (P<0.05) in serum corticosterone, testosterone, follicle-stimulating hormone and GnRH when compared with the control. Dex treatment at GD 15-21 and 1-21 significantly reduced (P<0.05) sperm motility and normal morphology in the F1 and F2 offspring. Maternal Dex treatment in rats during late gestation may disrupt sexual development markers in the F1 and F2 male offspring.

Maternal treatment with dexamethasone during lactation delays male puberty and disrupts reproductive functions via hypothalamic-pituitary-gonadal axis alterations.

The effects of maternal treatment with dexamethasone during lactation on pubertal timing, serum hormonal profile and sperm indices in the male offspring were assessed. Twenty lactating dams were divided into 4 groups (n=5). Group 1 was administered subcutaneously 0.02ml/100g/day normal saline at lactation days 1-21. Groups 2-4 were administered subcutaneously 100µg/kg/day dexamethasone (Dex) at lactation days 1-7, 1-14, and 1-21 respectively. Results showed that there was significant reduction in serum testosterone in the DexLD 1-7 (p<0.05), DexLD 1-14 (p<0.01) and DexLD 1-21 (p<0.001) relative to control. In addition there was a significant reduction in serum FSH and LH in the DexLD 1-7 (p<0.01), DexLD 1-14 (p<0.001) and DexLD 1-21 (p<0.001) when compared with the control. Treatment with dexamethasone during lactation significantly increased the days of preputial separation in the DexLD 1-7 (p<0.05), DexLD 1-14 (p<0.05) and DexLD 1-21 (p<0.001) relative to control. Maternal treatment with dexamethasone throughout lactation period also significantly reduced sperm counts (p<0.001), motility (p<0.01) and increased percentage abnormal sperm (p<0.001) in the offspring when compared with the control. In conclusion, maternal treatment with dexamethasone during lactation may induce delayed puberty and disrupt reproductive functions by altering activities at hypothalamic-pituitary-gonadal axis in the male offspring.

Changes in kidney function and oxidative stress biomarkers in offspring from dams treated with dexamethasone during lactation in Wistar rats.

BACKGROUND: The effects of maternal exposure to glucocorticoids during gestation on various organs in the offspring have been reported in literature. There is paucity of information on the effects of maternal glucocorticoids treatment during lactation on organ functions in the offspring. The present study was designed to investigate the changes in kidney function and oxidative stress biomarkers in offspring of dams treated with dexamethasone during lactation in Wistar rats METHODS: Twenty pregnant rats (180-200g) were divided into 4 groups (n=5). Group I was administered 0.02ml/100g/day of normal saline (subcutaneously, s.c) at lactation days 1-21 (control). Groups 2,3, and 4 were administered 100 µ/kg/day dexamethasone (Dex) (s.c) at lactation days 1-7 (Dexl-7),1-14(Dexl-14), and 1-21(Dexl-21) respectively. Evaluation of serum creatinine, urea and markers of oxidative stress in the kidney and histopathology of the kidney were carried out at 12 weeks of postnatal life. RESULTS: Serum creatinine and urea levels were. significantly (p<0.05) higher in the Dexl-7, DexI-14and Dexl-21 when compared with the control. Kidney MDA level was also significantly (p

Effects of Maternal Dexamethasone Exposure During Lactation on Metabolic Imbalance and Oxidative Stress in the Liver of Male Offsprings of Wistar Rats.

It has been reported in human and animal studies that early exposure to glucocorticoids could retard growth and subsequent development of cardio metabolic diseases. Chronic exposure to glucocorticoids induced oxidative stress. Therefore, the role of oxidative stress in some of the observed metabolic imbalance needs to be elucidated. This study examined the effects of lactational dexamethasone exposure on metabolic imbalance and oxidative stress marker in the liver of male offspring of exposed mother. Twenty lactating dams were divided into 4 groups of 5 animals each. Group 1 was administered 0.02 ml/100gbwt/day normal saline through lactation days 1-21. Group 2, 3, and 4 were administered 100 µg/kgbwt/day dexamethasone for lactation days 1-7, 1-14, and 1-21 respectively. The male offspring were thereafter separated and sacrificed at 12weeks of age for evaluation of lipid profile and oxidative stress marker in the liver. Results from this study indicate that Total Cholesterol (TC), Triglycerides (TAG) and LDL- cholesterol (LDL-C) were significantly  higher in the Dex 1-7, Dex 1-14 and Dex 1-21 groups when compared with the control. HDL-Cholesterol (HDL-C) was significantly reduced in the Dex 1-7, Dex 1-14 and Dex 1-21 groups relative to the control. Basal Fasting Blood Sugar (FBS) was also significantly higher in the Dex 1-14 and Dex 1-21 groups when compared with the control. Liver malondialdehyde was significantly higher in the Dex1-14 and Dex1-21 group compared to the control. However, liver catalase and SOD activity were all significantly lower in Dex 1-7, Dex 1-14 and Dex 1-21 groups relative to control. Liver protein was significantly lower in the Dex1-14 and Dex1-21 treatment groups when compared with the control. Findings from this study suggest that there is possible increase in metabolic imbalance in the offspring of mother exposed to dexamethasone during lactation and these effects may be secondary to increase oxidative stress in the liver.