Adansonia digitata L. fruit shell extract alleviates lead-induced neurotoxicity in mice via modulation of oxidative stress and a possible chelating activity.

Autor: Fannami IM; Department of Human Anatomy, Faculty of Basic Medical Sciences, University of Maiduguri, Borno state, Nigeria., Garba SH; Department of Human Anatomy, Faculty of Basic Medical Sciences, University of Maiduguri, Borno state, Nigeria., Chiroma SM; Department of Human Anatomy, Faculty of Basic Medical Sciences, University of Maiduguri, Borno state, Nigeria. Electronic address: musasamailachiroma@yahoo.com.
Jazyk: angličtina
Zdroj: Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) [J Trace Elem Med Biol] 2022 Dec; Vol. 74, pp. 127074. Date of Electronic Publication: 2022 Sep 13.
DOI: 10.1016/j.jtemb.2022.127074
Abstrakt: Background: Lead is a ubiquitous environmental heavy metal known to induce neurotoxicity. It has been postulated that substance with high antioxidant capacity could alleviate lead-induced neurotoxicity. Adansonia digitata fruit shell extract (ADFS) has been reported to have high phenolic contents and exerts antioxidant activity. This study investigated the effects of Adansonia digitata fruit shell extract on lead-induced neurotoxicity in mice.
Methods: Male balb/c mice (n = 7) were administered with Pb-acetate (50 mg/kg) 30 mins before ADFS (250 mg/kg and 500 mg/kg) or succimer (50 mg/kg) per orally for 28 days. Motor activities were evaluated on days 29 and 30 through horizontal bar and open field tests respectively. Further, spectrophotometry, atomic absorption spectrophotometry and haematoxylin and eosin staining were carried-out to determine the expression of oxidative stress biomarkers, level of lead concentration in the brain and histology of the cerebellum respectively.
Results: Lead acetate exposure significantly (p < 0.05) induced motor deficits in horizontal bar test and open field test, caused oxidative stress, high concentration of lead in the brain as well as histological aberration in the cerebellum. ADFS significantly (p < 0.05) reversed the motor deficits evident by increased muscle strength and number of lines crossed. Further, ADFS significantly reversed oxidative stress evident by increased levels of SOD, CAT and GSH and decreased level of MDA. There was also significant (p < 0.05) decrease in brain lead concentration as well as reduced cerebellar cells death.
Conclusion: Findings suggest that ADFS attenuated motor deficits via inhibition of oxidative stress and chelating activity which is comparable to succimer. Hence, ADFS should be explored for possible development of chelating agent against lead and other heavy metals toxicity.
Competing Interests: Declaration of Competing Interest Authors declare no conflict of interest.
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Databáze: MEDLINE
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