scholarly journals Recovery of Prenatal Baicalein Exposure Perturbed Reproduction by Postnatal Exposure of Testosterone in Male Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Sridevi Vaadala ◽  
Naveen Ponneri ◽  
Venkata Shashank Karanam ◽  
Sri Bhashyam Sainath ◽  
Pamanji Sreenivasuala Reddy ◽  
...  

Baicalein (BC), a flavonoid, which lacks the qualities of reproductive health and shows adverse effects, is tested in this study. Inseminated mice were injected with 30, 60, and 90 mg BC/Kg body weight on gestation days 11, 13, 15, and 17. The F1 BC-exposed males of each dosage were divided into six groups. First three groups (n = 6 from each BC dosage) were used for assessment of reproductive performance, the others (n = 4 from each BC dosage) were administered with testosterone 4.16 mg/kg body weight on postnatal days 21, 31, and 41. The reproductive health of adult F1 males at the age of 55 and 60 was tested. Prenatal BC exposure showed reduced fertility after cohabitation with control females. The BC exposure significantly reduced the body weight, tissue indices, and sperm parameters (motility, count, viability, and daily sperm count) and altered the sperm membrane in a hypoosmotic swelling test. A downward trend was observed in testicular steroidogenic marker enzymes (3β- and 17β-steroid dehydrogenases) and serum testosterone, whereas increase in serum titers of FSH and LH along with altered the testicular histology. Conversely, testosterone (4.16 mg/kg body weight) partially recovered reduced male reproductive health by BC. BC impaired male reproductive health due to low levels of testosterone is reverted by external testosterone is evidenced in this study.

2002 ◽  
Vol 21 (1) ◽  
pp. 37-41 ◽  
Author(s):  
N Pant ◽  
SP Srivastava

A study was conducted with nitrate to assess the testicular and spermatotoxic effects in mice at doses to which human beings are exposed as well as at higher dose levels in the drinking water. Potassium nitrate was administered to mice at dose levels 90, 200, 500, 700 and 900 ppm for 35 days. There was no difference in the uptake of water in control and treated animals. The amount of nitrate intake// mouse///day calculated on the basis of water intake in the different groups ranged from 22.5 to 27, 50 to 60, 125 to 150, 175 to 210 and 225 to 270 mg///kg body weight. No changes were evident in the body weight, testicular, epididymal and accessory organ weight at all the dose levels tested, although a decline in sperm count and sperm motility along with an increase in abnormal sperm was noticed at 900 ppm. The activity of marker testicular enzymes, mainly 17-β hydroxysteroid dehydrogenase (17-β HSD) and figlutamyl transpeptidase (fi-GT), associated with specific cell types were altered. Histopathological changes including atrophy and disturbed spermatogenesis were observed only at the 900-ppm dose level. In conclusion, we can say that the testicular and spermatotoxic effects are observed only at the highest dose level, which is not likely to be encountered in the drinking water.


PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e7192 ◽  
Author(s):  
Rui Li ◽  
Hao Li ◽  
Ke Rao ◽  
Kang Liu ◽  
Yan Zhang ◽  
...  

Background The growth and function of seminal vesicle are dependent on androgen. This study was conducted to investigate the role of oxidative stress in castration-induced seminal vesicle atrophy and to explore the effects of curcumin, an antioxidant extracted from rhizome of turmeric, on seminal vesicle of castrated mice. Methods C57BL/6J mice were randomly divided into three groups: control, castration, and castration with curcumin (n = 10 for each group). After surgical castration, mice in the curcumin treatment group received intragastric administration of curcumin at 100 mg/kg body weight for 4 weeks, whereas mice in the other two groups were treated with olive oil. After that, the body weight, seminal vesicle weight and serum testosterone of mice were measured. Apoptosis and oxidative stress levels in seminal vesicle were also determined. Results After castration, both the weight and size of seminal vesicle decreased dramatically. The expression of three NADPH oxidase (NOX) subtypes: NOX1, NOX2 and NOX4, increased in seminal vesicle of castrated mice, resulting in high level oxidative stress. The ratio of Bax to Bcl-2 was also elevated after castration, accompanied by enhanced caspase3 activity. Additionally, castration increased the number of apoptotic cells in seminal vesicle. Curcumin treatment could inhibit the expression of NOX1, NOX2 and NOX4, decreasing oxidative stress and apoptosis. The atrophy of seminal vesicle caused by castration was ameliorated by curcumin. Conclusion Castration could cause atrophy of seminal vesicle probably via inducing oxidative stress. Curcumin treatment could reduce the oxidative stress in seminal vesicle by decreasing the expression of NOX1, NOX2 and NOX4, thereby ameliorating apoptosis and atrophy of seminal vesicle. Oxidative stress might play a role in castration-induced seminal vesicle atrophy.


2020 ◽  
Vol 26 (1) ◽  
pp. 53-64
Author(s):  
Peter Kelechi Ajuogu ◽  
Mohammed AK Al-Aqbi ◽  
Robert A Hart ◽  
Mitchell Wolden ◽  
Neil A Smart ◽  
...  

Background: Studies have shown that the amount of protein in the diet affects the hypothalamic-pituitary-testis axis and sub-optimal quantity reduces male fertility potential in both animals and humans. However, individual research reports on the factors associated with male infertility are collectively uncharacterized. Aim: We systematically reviewed, and meta-analysed animal (rats) studies on the effect of low protein diet on factors associated with male infertility. Methods: PubMed Central, EMBASE and Scopus databases were searched from inception to 30 March 2019 for the study concepts and related keywords in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) protocol. Data on the outcome measures were extracted and pooled across trials using random-effects model and expressed as mean differences (MD) at a 95% confidence interval (CI). Results: Twelve trials identified from 3327 studies, met our inclusion criteria in the comparison of a low protein diet (2–10% protein) vs control protein diet (17–23% protein). The results showed that a low protein diet caused a significant reduction in the body weight ( P = 0.0001) testis weight ( P = 0.0001), seminal vesicle weight ( P = 0.0003), epididymis weight P = 0.02), serum testosterone ( P = 0.001) and follicle-stimulating hormone (FSH) concentrations ( P = 0.04) compared with the control treatments. No effect on luteinizing hormone (LH) plasma concentration ( P = 0.13) was observed. Conclusion: This study revealed that low protein diet caused significant reductions in body weight, testis, epididymis and seminal vesicle weights, serum testosterone and FSH concentration in rats. We infer that sub-optimal protein consumption reduces the gonadal and endocrine function, and consequently male infertility.


Author(s):  
V. Madhavi ◽  
U. Kanchana Ganga ◽  
S. B. Sainath ◽  
B. Kishori

Aims: The present study was aimed to investigate the protective role of ginger against acephate-induced testicular toxicity in adult rats. Methodology: Rats were allocated into four groups where animals in group I served as controls, while animals in group II, III and group IV were treated as experimental rats. Rats in groups II, III and IV were treated with acephate (50mg/kg body weight), ginger (100mg/kg body weight) and combination of both acephate and ginger, respectively over a period of 60 days. After completion of experimental period sperm count, sperm viability, sperm motility, sperm membrane integrity, testicular steroidogenic marker enzymes (3β-HSD and 17β-HSD, serum testosterone and testicular architecture was performed in both control and experimental rats. Results: Relative weights of reproductive organs, sperm count, sperm viability, sperm motility and sperm membrane integrity were significantly decreased in acephate treated rats over controls. Acephate administration also reduced the circulatory levels of testosterone associated with a significant reduction in the testicular steroidogenic marker enzymes (3β-HSD and 17β-HSD) in rats. The testicular architecture was disrupted in acephate intoxicated rats. In contrast, ginger administration significantly recovered the acephate-induced suppressed selected reproductive parameters with increased circulatory levels of testosterone and restoration of sperm endpoints in as compared to acephate alone treated rats. No significant changes were observed in any of the selected reproductive endpoints in ginger treated rats as compared to controls. Conclusion: The results can be concluded that supplementation of ginger mitigates the negative effects of acephate on male reproductive health via amelioration of testicular setroidogenesis and spermatogenesis and epididymal sperm maturation events in rats.


2019 ◽  
Vol 5 (2) ◽  
pp. 47-54
Author(s):  
Dian Anggraini ◽  
Sutyarso Sutyarso ◽  
M. Kanedi ◽  
Hendri Busman

Paraquat is one of the chemicals that contributes to increasing pollution Indonesia. The careless use of paraquat can increase production of ROS (Reactive Oxygen Species), resulting in damage to a wide range of vital organs and reproductive system disorders such as infertility. ROS in the body can be captured by antioxidants. Red Ginger contains high antioxidants because there are active phenolic compounds such as gingerol, shagaol, zingeron, ginggerdiol, and zingibren which are proven to protect body cells from damage caused by ROS. This study was aimed to test the effectiveness of red ginger extract (Zingiber officinale Roxb. Var. Rubrum) on the quantity and quality of sperm in male mice (Mus musculus L.) induced by paraquat dichloride.This research uses a completely randomized design and is divided into six treatment groups with each four replications: K1 as the control group (only given H2O); K2 (paraquat induced a dose of 20 mg/kg Body Weight (BW) without the administration of the test substances); K3; K4; K5 (paraquat induced a dose of 20 mg/kg Body Weight (BW) and was given a red ginger extract at a dose of consecutive succession 6 mg / ml, 12 mg / ml, 18 mg / ml) and K6 (Only given a test material the red ginger extract as much as 18 mg / ml). Paraquat was given 2 times a week for 21 days and the red ginger extract was given for 35 days. The results of analysis by One-way ANOVA followed LSD at 5% significance level showed the ethanolic extract of red ginger can increase the sperm count, motility, viability and Morphology sperm of mice induced by the paraquat diklorida.


2018 ◽  
Author(s):  
Liudmila Vyacheslavovna Fomina ◽  
Duy Bac Nguyen ◽  
Xuan Phong Pham ◽  
Hoang Ngan Nguyen

The study was conducted to evaluate the effects of improving sperm production with the use of Vietnamese deer antler velvet powder on a white rat, whose sperm count was decreased by valproic acid. The findings showed that using deer antler velvet powder at doses of 127.5 mg/kg/24 hrs, 255 mg/kg/24 hrs and 510 mg/kg/24 hrs for 6 weeks on the male rat having a low sperm count recovered the research parameters (serum testosterone levels, sperm quantity and quality, reproductive organs and testicular histology).


Reproduction ◽  
2009 ◽  
Vol 137 (3) ◽  
pp. 439-448 ◽  
Author(s):  
C Harini ◽  
S B Sainath ◽  
P Sreenivasula Reddy

The present study aimed to examine whether transplacental exposure to progesterone caused male reproductive abnormalities and whether the changes can be reversed after testosterone administration. Progesterone was injected to mice on day 1, 3, and 7 of pregnancy. The male pups (F1 generation) were allowed to grow for 50 days and assessed for reproductive performance. Gestational exposure to progesterone (7 mg/kg body weight) resulted in significant body weight gain with a decrease in reproductive tissue indices in mice. Total sperm count, viable sperm, and motile sperm decreased in experimental mice. Hypo-osmotic swelling test revealed that experimental mice sperm membrane integrity was severely altered. The activity levels of testicular steroidogenic marker enzymes (hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase cluster (HSD3B) and hydroxysteroid (17-beta) dehydrogenase 1 (HSD17B)) decreased significantly in mice exposed to progesterone during embryonic development when compared with the controls. The levels of serum testosterone decreased with an increase in serum FSH and LH in mice exposed to progesterone during embryonic development. Prenatal exposure to progesterone caused significant reduction in the number of spermatozoa and increase in the lumen of seminiferous tubule. The experimental mice that cohabited with normal females showed fertility reduction. Administration of testosterone (4.16 mg/kg body weight) on postnatal day 20, 30, and 40 to progesterone-exposed prenates resulted in recovery of progesterone-induced suppressed male reproduction. It is suggested that the impairment of male reproduction in mice exposed to progesterone during embryonic development could be mediated through the inhibition of testosterone production. These results also indicate thatin uteroexposure to progesterone affects male reproduction and that supplementation of testosterone restores the suppressed male reproduction.


2018 ◽  
Vol 475 (22) ◽  
pp. 3535-3560 ◽  
Author(s):  
Bruno P. Moreira ◽  
Mariana P. Monteiro ◽  
Mário Sousa ◽  
Pedro F. Oliveira ◽  
Marco G. Alves

Obesity stands as one of the greatest healthcare challenges of the 21st century. Obesity in reproductive-age men is ever more frequent and is reaching upsetting levels. At the same time, fertility has taken an inverse direction and is decreasing, leading to an increased demand for fertility treatments. In half of infertile couples, there is a male factor alone or combined with a female factor. Furthermore, male fertility parameters such as sperm count and concentration went on a downward spiral during the last few decades and are now approaching the minimum levels established to achieve successful fertilization. Hence, the hypothesis that obesity and deleterious effects in male reproductive health, as reflected in deterioration of sperm parameters, are somehow related is tempting. Most often, overweight and obese individuals present leptin levels directly proportional to the increased fat mass. Leptin, besides the well-described central hypothalamic effects, also acts in several peripheral organs, including the testes, thus highlighting a possible regulatory role in male reproductive function. In the last years, research focusing on leptin effects in male reproductive function has unveiled additional roles and molecular mechanisms of action for this hormone at the testicular level. Herein, we summarize the novel molecular signals linking metabolism and male reproductive function with a focus on leptin signaling, mitochondria and relevant pathways for the nutritional support of spermatogenesis.


Author(s):  
Meltem Mermer ◽  
Yasemin Akdevelioğlu

Obesity causes many health problems as well as having negative effects on fertility. There is a multifaceted relationship between obesity and male infertility. Male fertility is associated with sperm concentration, motility and morphology. Testosterone (total and free) and gonadotropin levels were low and estrogen levels were found to be high in obese men. The decrease in androgen levels varies based on the degree of obesity. High body mass index is inversely related to total sperm count, sperm concentration, sperm morphology and number of motile sperm. Leptin and ghrelin are hormones that influence body weight regulation and eating behaviors. Serum leptin level, which is high in obese infertile men, showed a significant positive correlation with abnormal sperm morphology, serum FSH, LH, prolactin level and showed a significant negative correlation with sperm concentration, sperm motility and serum testosterone level. Further research is needed on the effects of ghrelin levels on male infertility. The relationship between obesity and erectile dysfunction can be explained by decreased testosterone levels and elevation of some proinflammatory cytokine levels. Decreased physical activity due to obesity, long-term sitting increases testicular temperature and affects sperm production negatively. There is a multifaceted relationship between obesity, metabolic syndrome and type 2 diabetes and serum testosterone and SHBG. Diet and exercise showed improvement in testosterone levels and sperm concentration due to decreased body weight. However, studies on this subject are extremely limited. The possible effects of weight loss on successful infertility treatment of obese men should not be ignored.


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