Flavonoid fractions of diosmin and hesperidin mitigate lead acetate-induced biochemical, oxidative stress, and histopathological alterations in Wistar rats

Author(s):  
Ibrahim Yusuf Lamidi ◽  
Hudu Garba Mikail ◽  
Sani Adamu ◽  
Isaac Oluwatobi Akefe ◽  
Mohammed Bashir Tijjani ◽  
...  
2015 ◽  
Vol 31 (1) ◽  
pp. 37-44 ◽  
Author(s):  
Wahab Imam Abdulmajeed ◽  
Habeeb Bolakale Sulieman ◽  
Maymunah Oloruntosin Zubayr ◽  
Aminu Imam ◽  
Abdulbasit Amin ◽  
...  

2022 ◽  
Vol 16 (1) ◽  
pp. 34-42
Author(s):  
Omotayo B. Ilesanmi ◽  
◽  
Eni-yimini Solomon Agoro ◽  

Background: Trevo is a nutritional supplement with numerous bioactive natural products, with detoxifying and antioxidant properties. The purpose of this study was to investigate the ability of Trévo to protect against oxidative stress induced by lead in the kidneys of male Wistar rats. Methods: Thirty-five healthy male Wistar rats were divided into five groups of seven rats each, using a randomized design. I=control; II=15 mg/kg of lead acetate (PbA); III=2 ml/kg of trevo+PbA; IV=5 ml/kg of trevo+PbA; V=5 ml/kg of trevo. Animals were treated with trevo for five days before co-administration with lead intraperitoneally for 10 consecutive days. Animals were sacrificed 24hr after the last administration, blood samples were collected via cardiac puncture, and processed for assessment of urea, creatinine, and uric acid (UA), while the kidney samples were excised and processed for the following biochemical assays: Malondialdehyde (MDA), Glutathione-S-Transferase (GST), Catalase (CAT), Superoxide Dismutase (SOD), and Reduced Glutathione (GSH). Results: Injection of PbA caused a significant increase in the serum levels of urea, creatinine, and uric acid, and a significant increase (P<0.001) in the MDA concentration, and decreases in GSH concentration, CAT, SOD, and GST activities (P<0.05) as compared to the controls. Pretreatment with trevo prevented the oxidative stress induced by lead acetate in the kidney tissue samples and improve the renal function. The protective effect was evident at 5 ml/kg of trevo. Conclusion: The results showed that trevo was nephroprotective against lead toxicity and the activity might be linked to the presence of numerous antioxidant phytochemicals present in trevo.


2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Temidayo Omobowale ◽  
Oyagbemi Ademola ◽  
Adebowale Saba ◽  
Stephen Akinrinde ◽  
Temilade Daramola ◽  
...  

2019 ◽  
Vol 17 (6) ◽  
pp. 651-662 ◽  
Author(s):  
Mohammad Yahya Karimi ◽  
Iman Fatemi ◽  
Heibatullah Kalantari ◽  
Mohammad Amin Mombeini ◽  
Saeed Mehrzadi ◽  
...  

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Vivian Atuadu ◽  
Ben-Azu Benneth ◽  
John Oyem ◽  
Emmanuel Esom ◽  
Chris Mba ◽  
...  

AbstractObjectivesAdansonia digitata L. is popularly known for the management of various neurological diseases in ethno-medicine. Studies have shown that lead toxicity is a possible risk factor for early onset of neurodegenerative disease. Hence, this study was designed to evaluate the effect of A. digitata aqueous leaf extract (ADALE) against lead-induced oxidative stress and histo-architectural changes in the prefrontal cortex of adult Wistar rats.MethodsSaline (10 mL/kg), ADALE (500 and 1000 mg/kg) and EDTA (55 mg/kg) were pretreated orally 30 min prior to lead acetate (LA) (120 mg/kg) administration to male Wistar rats (n=7) for 21 days. Thereafter, standard biochemical (superoxide dismutate, catalase, glutathionxe and malondialdehyde), histological (H&E) and histochemical assessment (crystyl fast violet stain for nissil substance) were carried out in the prefrontal cortex.ResultsADALE significantly (p<0.05) reversed LA-induced oxidative stress, as evidenced by increased catalase, superoxide dismutase and oxidized glutathione levels, and decreased malondialdehyde concentration in the prefrontal cortex. Also, the increase chromatolysis and neuronal pyknosis of the pyramidal neurons of the prefrontal cortex were significantly attenuated by ADALE.ConclusionsThe result of this study showed that A. digitata aqueous leaf extract attenuated lead acetate-induced cortical neurodegeneration via inhibition of oxidative stress.


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