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      Honey supplemented with Vitamin C prevents dyslipidaemia and oxidative stress induced by exposure to lead acetate in Wistar rats

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          Abstract

          Objectives:

          Lead is an environmental toxicant known to cause dyslipidaemia through oxidative stress damage. The therapeutic potential of honey has widely been reported. However, there is a paucity of reports on its effects on lipid profile in Wistar rats exposed to lead.

          Materials and Methods:

          The effects of honey on antioxidants and lipid profile indicators were studied in 25 male Wistar rats. The rats were randomly assigned to one of the five groups ( n = 5) as follows: Group I served as the control and received deionised water; Group II served as a lead acetate group (40 mg/kg bw) and Groups III, IV and V served as lead acetate groups coadministered with honey (1 mL/kg bw), Vitamin C (100 mg/kg bw) and honey+Vitamin C, respectively. The treatments were orally administered for 28 days. Body and liver weights were determined using an analytical weighing balance. Glucose and lead concentration, superoxide dismutase (SOD), total antioxidant capacity (TAC), malondialdehyde (MDA), and the lipid profile indicators were determined using spectrophotometry. The liver histology was assessed by haematoxylin and eosin staining techniques. Statistical analysis was done using analysis of variance, and the results were expressed as mean ± S.E.M. at P < 0.05.

          Results:

          Body weight, SOD, and TAC increased significantly in the treatment groups compared to lead acetate only. However, lead, glucose concentration, MDA, total cholesterol, triglycerides, HDL, and LDL decreased significantly in the treatment groups compared to lead acetate only. Normal histoarchitecture of the liver was seen in the treatment groups compared to lead acetate, which showed areas of inflammation.

          Conclusion:

          These findings imply that honey prevents dyslipidaemia which is a risk factor for metabolic diseases.

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          Most cited references55

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          The role of superoxide anion in the autoxidation of epinephrine and a simple assay for superoxide dismutase.

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            Free radicals, metals and antioxidants in oxidative stress-induced cancer.

            Oxygen-free radicals, more generally known as reactive oxygen species (ROS) along with reactive nitrogen species (RNS) are well recognised for playing a dual role as both deleterious and beneficial species. The "two-faced" character of ROS is substantiated by growing body of evidence that ROS within cells act as secondary messengers in intracellular signalling cascades, which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. The cumulative production of ROS/RNS through either endogenous or exogenous insults is termed oxidative stress and is common for many types of cancer cell that are linked with altered redox regulation of cellular signalling pathways. Oxidative stress induces a cellular redox imbalance which has been found to be present in various cancer cells compared with normal cells; the redox imbalance thus may be related to oncogenic stimulation. DNA mutation is a critical step in carcinogenesis and elevated levels of oxidative DNA lesions (8-OH-G) have been noted in various tumours, strongly implicating such damage in the etiology of cancer. It appears that the DNA damage is predominantly linked with the initiation process. This review examines the evidence for involvement of the oxidative stress in the carcinogenesis process. Attention is focused on structural, chemical and biochemical aspects of free radicals, the endogenous and exogenous sources of their generation, the metal (iron, copper, chromium, cobalt, vanadium, cadmium, arsenic, nickel)-mediated formation of free radicals (e.g. Fenton chemistry), the DNA damage (both mitochondrial and nuclear), the damage to lipids and proteins by free radicals, the phenomenon of oxidative stress, cancer and the redox environment of a cell, the mechanisms of carcinogenesis and the role of signalling cascades by ROS; in particular, ROS activation of AP-1 (activator protein) and NF-kappaB (nuclear factor kappa B) signal transduction pathways, which in turn lead to the transcription of genes involved in cell growth regulatory pathways. The role of enzymatic (superoxide dismutase (Cu, Zn-SOD, Mn-SOD), catalase, glutathione peroxidase) and non-enzymatic antioxidants (Vitamin C, Vitamin E, carotenoids, thiol antioxidants (glutathione, thioredoxin and lipoic acid), flavonoids, selenium and others) in the process of carcinogenesis as well as the antioxidant interactions with various regulatory factors, including Ref-1, NF-kappaB, AP-1 are also reviewed.
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              Is Open Access

              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
                Indian Journal of Physiology and Pharmacology
                IJPP
                Scientific Scholar
                2582-2799
                0019-5499
                2022
                February 25 2022
                : 65
                : 229-236
                Affiliations
                [1 ]Department of Physiology, University of Medical Sciences, Ondo City, Nigeria,
                [2 ]Department of Physiology, Edo State University, Edo, Nigeria,
                Article
                10.25259/IJPP_445_2021
                b47508a3-8ca4-497e-8226-4d320b78d7a7
                © 2022
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