ETHANOLIC ROOT EXTRACTS OF RAUWOLFIA VOMITORIA AMELIORATES REPRODUCTIVE TOXICITY AND OXIDATIVE STRESS INDUCED BY ALUMINIUM CHLORIDE IN RATS.

Author(s):  
Arhoghro E. M.
2010 ◽  
Vol 196 ◽  
pp. S230
Author(s):  
G. Castro ◽  
L. Buthet ◽  
S. Fanelli ◽  
C. Rodríguez De Castro ◽  
M. Costantini ◽  
...  

2019 ◽  
Vol 316 ◽  
pp. 60-72 ◽  
Author(s):  
Mohammad Mehdi Ommati ◽  
Omid Farshad ◽  
Hossein Niknahad ◽  
Mohammad Reza Arabnezhad ◽  
Negar Azarpira ◽  
...  

2019 ◽  
Vol 35 (3) ◽  
pp. 228-238 ◽  
Author(s):  
Yu-Qin Shi ◽  
Guo-Qing Fu ◽  
Jing Zhao ◽  
Shen-Zhou Cheng ◽  
You Li ◽  
...  

Di(2-ethylhexyl)phthalate (DEHP) is a typical endocrine-disrupting chemical and reproductive toxicant. Although previous studies have attempted to describe the mechanism by which DEHP exposure results in reproductive dysfunction, few studies focused on puberty, a critical period of reproductive development, and the increased susceptibility to injury in adolescents. To elucidate the mechanism underpinning the testicular effects of DEHP in puberty, we sought to investigate the JAZF1/TR4 pathway in the testes of pubertal rats. Specifically, we focused on the role of the JAZF1/TR4 pathway in male reproduction, including the genes JAZF1, TR4, Sperm 1, and Cyclin A1. In the present study, rats were exposed to increasing concentrations of DEHP (0, 250, 500, and 1000 mg/kg/day) by oral gavages for 30 days. Then we assayed testicular zinc and oxidative stress levels. Our results indicated that DEHP exposure could lead to oxidative stress and decrease the contents of testicular zinc. Additionally, significant morphological changes and cell apoptosis were observed in testes exposed to DEHP, as identified by hematoxylin and eosin staining and the terminal deoxynucleotidyl transferase-mediated nick and labeling assay. By measuring the expression levels of the above relevant genes by qPCR, we found the DEHP-induced increased expression of JAZF1 and decreased expression of TR4, Sperm 1, and Cyclin A1. Therefore, we have demonstrated that in vivo exposure to DEHP might induce reproductive toxicity in pubertal male rats through the JAZF1/TR4 pathway and oxidative stress.


PLoS ONE ◽  
2017 ◽  
Vol 12 (4) ◽  
pp. e0175990 ◽  
Author(s):  
Merve Baysal ◽  
Sinem Ilgin ◽  
Gozde Kilic ◽  
Volkan Kilic ◽  
Seyda Ucarcan ◽  
...  

Author(s):  
Ganiyu Oboh ◽  
Adeniyi A. Adebayo ◽  
Ayokunle O. Ademosun

Abstract Background In Nigerian traditional medicine, Rauwolfia vomitoria has been reported to be useful in the management of various human diseases, but there is no relevant information to substantiate its involvement in managing diseases arising from vascular dysfunction and oxidative stress. However, this study sought to investigate the antioxidant property of R. vomitoria and its effect on phophodiesterase-5 activity in vitro. Methods The antioxidant property was assessed through ferric-reducing antioxidant power (FRAP), copper chelation, and ABTS radical-scavenging activity. In addition, the effect of R. vomitoria on phosphodiesterase-5 (PDE-5) activity was assessed in vitro. Furthermore, analysis of phenolic compounds present in R. vomitoria was carried out using high-performance liquid chromatography (HPLC). Results The findings in this study revealed that R. vomitoria inhibited PDE-5 in a dose-dependent manner (IC50 = 252.42 μg/mL). Furthermore, the antioxidant activity of R. vomitoria was established through FRAP (19.68 mg AAE/g), ABTS radical-scavenging ability (74.25 mmol TEAC/g), and Cu2+-chelating ability (IC50 = 0.13 mg/mL). Conclusions The antioxidant property of R. vomitoria and its inhibitory effect on PDE-5 could be useful in the management of diseases arising from vascular dysfunction and oxidative stress.


2021 ◽  
Vol 6 (3) ◽  
pp. 113-119
Author(s):  
Yidjeu Nana Aristide ◽  
◽  
Nantia Akono Edouard ◽  
Tchagnhe Fotsing Milwilie ◽  
Guiekep Nounamo Jemima ◽  
...  

The soil and agricultural products pollution by nickel represents an important public health risk in agrarian areas such as the Dschang in Cameroon. This study was designed to evaluate the reproductive toxicity and oxidative stress potential of nickel chloride in male guinea pig. Four groups of adult male guinea pigs were orally treated with nickel chloride at doses of 0, 17.50, 26.25 and 52.50 mg/kg bw for 90 days. At the end of the experimental period, all animals were sacrificed, and blood samples and vital organs were collected for different analysis. Treatment of male guinea pigs with 52.50 mg/kg nickel chloride resulted in increased kidney weight and volume and decreased weights of the sex accessory glands (seminal vesicle + prostate + coagulating glands), epididymis and vas deferens. The 52.50 mg/kg dose of nickel chloride decreased (p<0.05) the animal’s sperm mobility, number and viability, while it increased (p<0.05) sperm micro and macrocephalies. Assessment of biochemical parameters of toxicity revealed increase (p<0.05) of serum creatinine and aminotransferases activities in the nickel chloride-exposed guinea pigs (52.50 mg/kg). The nickel chloride (52.50 mg/kg) also promoted oxidative stress, through decrease (p<0.05) of superoxide dismutase and catalase activities, as well as increase (p<0.05) in lipid peroxydation. In addition, histology of testis revealed disrupted germ cell arrangement, decreased concentration of sperms in the lumen of the seminiferous tubules and degraded germinal epithelium in the animals exposed to nickel chloride. In conclusion, results obtained in this study revealed that nickel chloride perturbs male reproductive system and induced oxidative stress.


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