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      Neuromodulatory roles of PIPER GUINEENSE and honey against Lead-Induced neurotoxicity in social interactive behaviors and motor activities in rat models

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          Abstract

          Background

          Piper guineense and honey contain antioxidative, anti-inflammatory, and antimicrobial properties that can help restore neuronal and other cell damage. To investigate the neuromodulatory roles of p. guineense and honey against lead toxicity on the hippocampus and cerebellum, impairing social behaviors and motor activities.

          Methodology

          Thirty Wistar rats were separated into six groups of five rats each, marked with dye. Group A served as control; B was untreated lead; C was a medium dose of the extract (50 mg/kg) and honey (1000 mg/kg); D was a high dose of the extract (80 mg/kg) and honey (1500 mg/kg); E received extract (80 mg/kg), and F received honey (1500 mg/kg). All groups received 110 mg/kg of lead orally, except the control. Social interaction, antidepressant effects, and motor activities were studied using a sociability chamber (SC), Forced Swim Test (FST), and String methods. A blood sample was used to evaluate glutathione peroxidase (GPx) and glutathione oxide transaminase (GOT), while the lipid level was estimated using cerebellar homogenate. Neuronal damage, vacuolation, necrosis, cell degeneration, and alterations in both hippocampus and cerebellum marked untreated group, with decreased GPx and GOT activities followed by impaired motor activities, social behavior, memory, and motivation. Using SCT, group B spent significantly lesser time (47.60 ± 47.60) with stranger 1 compared to A (138.20 ± 34.05), while group C spent considerably more time with stranger 1 (86.80 ± 30.32) than group B at P ≥ 0.05. The treatment increased the enzyme level and restored histoarchitecture ( Figures 112), improving motor activities, social behavior, memory, motivation, and social affiliation ( Tables 3, 4, 2, and 6). The extract and honey may be helpful as neuromodulators in lead toxicity in a dose-dependent manner.

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          Most cited references39

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          Behavioural phenotyping assays for mouse models of autism.

          Autism is a heterogeneous neurodevelopmental disorder of unknown aetiology that affects 1 in 100-150 individuals. Diagnosis is based on three categories of behavioural criteria: abnormal social interactions, communication deficits and repetitive behaviours. Strong evidence for a genetic basis has prompted the development of mouse models with targeted mutations in candidate genes for autism. As the diagnostic criteria for autism are behavioural, phenotyping these mouse models requires behavioural assays with high relevance to each category of the diagnostic symptoms. Behavioural neuroscientists are generating a comprehensive set of assays for social interaction, communication and repetitive behaviours to test hypotheses about the causes of autism. Robust phenotypes in mouse models hold great promise as translational tools for discovering effective treatments for components of autism spectrum disorders.
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            Toxic metals and oxidative stress part I: mechanisms involved in metal-induced oxidative damage.

            Toxic metals (lead, cadmium, mercury and arsenic) are widely found in our environment. Humans are exposed to these metals from numerous sources, including contaminated air, water, soil and food. Recent studies indicate that transition metals act as catalysts in the oxidative reactions of biological macromolecules therefore the toxicities associated with these metals might be due to oxidative tissue damage. Redox-active metals, such as iron, copper and chromium, undergo redox cycling whereas redox-inactive metals, such as lead, cadmium, mercury and others deplete cells' major antioxidants, particularly thiol-containing antioxidants and enzymes. Either redox-active or redox-inactive metals may cause an increase in production of reactive oxygen species (ROS) such as hydroxyl radical (HO.), superoxide radical (O2.-) or hydrogen peroxide (H2O2). Enhanced generation of ROS can overwhelm cells' intrinsic antioxidant defenses, and result in a condition known as "oxidative stress". Cells under oxidative stress display various dysfunctions due to lesions caused by ROS to lipids, proteins and DNA. Consequently, it is suggested that metal-induced oxidative stress in cells can be partially responsible for the toxic effects of heavy metals. Several studies are underway to determine the effect of antioxidant supplementation following heavy metal exposure. Data suggest that antioxidants may play an important role in abating some hazards of heavy metals. In order to prove the importance of using antioxidants in heavy metal poisoning, pertinent biochemical mechanisms for metal-induced oxidative stress should be reviewed.
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              Lead toxicity: a review

              Lead toxicity is an important environmental disease and its effects on the human body are devastating. There is almost no function in the human body which is not affected by lead toxicity. Though in countries like US and Canada the use of lead has been controlled up to a certain extent, it is still used vehemently in the developing countries. This is primarily because lead bears unique physical and chemical properties that make it suitable for a large number of applications for which humans have exploited its benefits from historical times and thus it has become a common environmental pollutant. Lead is highly persistent in the environment and because of its continuous use its levels rise in almost every country, posing serious threats. This article reviews the works listed in the literature with recent updates regarding the toxicity of lead. Focus is also on toxic effects of lead on the renal, reproductive and nervous system. Finally the techniques available for treating lead toxicity are presented with some recent updates.
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                Author and article information

                Journal
                AIMS Neurosci
                AIMS Neurosci
                neurosci
                AIMS Neuroscience
                AIMS Press
                2373-8006
                2373-7972
                15 November 2022
                2022
                : 9
                : 4
                : 460-478
                Affiliations
                [1] Department of Anatomy, Faculty of Basic Medical Sciences, College of Medicine, Alex Ekwueme Federal University Ndufu-Alike, Ikwo (AE-FUNAI), Ebonyi State, PMB 1010, Nigeria
                Author notes
                * Correspondence: E-mail: euchewa1@ 123456gmail.com ; Tel: +2348172628746 or +2347061644732.
                Article
                neurosci-09-04-026
                10.3934/Neuroscience.2022026
                9826751
                c219be4f-3932-4629-ab46-ddd1ab320fe5
                © 2022 the Author(s), licensee AIMS Press

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/4.0)

                History
                : 25 July 2022
                : 30 October 2022
                : 1 November 2022
                Categories
                Research Article

                lead aacetate,behavior,motor activities,neuromodulator,neurotoxicity,social interaction

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