Abstract
Heavy metal toxicity contributes to liver and kidney dysfunction and damage through oxidative stress mechanisms; however, from previous studies, extracts from the Vernonia amygdalina plant have shown to possess potent antioxidant properties. This study was aimed at uncovering the potential ameliorative effects of ethanolic extract from Vernonia amygdalina plant in heavy metal toxicity-induced liver and kidney dysfunction. For this study, 44 Sprague Dawley rats were divided into three groups. The control group received a basal diet and water only while the treatment groups received varied dosages of the heavy metals. The copper (Cu) and lead (Pb) groups had five subgroups. The Cu only and Cu recovery subgroups were administered with 16 mg/kg Cu intraperitoneally daily for 14 days, whereas the Pb only and Pb recovery subgroups were administered with 13 mg/kg Pb intraperitoneally daily for 14 days. Subsequently, the Pb only and Cu only subgroups were sacrificed. The three Pb and Cu treatment subgroups received oral graded doses (100 mg/kg, 200 mg/kg, and 300 mg/kg) of the extract for 21 days. The Cu recovery and Pb recovery subgroups were left to recover for 21 days. After histological examinations, the Pb and Cu pretreatment groups showed evidence of focal necrosis accompanied by inflammatory cell infiltrations. The serum levels of liver biomarkers AST, ALT, and GGT, as well as urea and creatinine, were significantly elevated (P=0.01) following copper and lead exposure. Upon posttreatment of the rats with the extract, the physiological levels of the biomarkers were restored and tissue architecture of the organs improved. Thus, the ethanolic extract of Vernonia amygdalina is capable of ameliorating the effects of heavy metal toxicity through potent antioxidative mechanisms.
Highlights
Heavy metals are defined as metallic elements that have a relatively high density compared to water
Heavy metals are well known for inducing oxidative stress. e mechanisms they apply in inducing oxidative stress include the production of reactive oxygen species (ROS), depletion of intracellular antioxidant stores and free radical scavengers, and inhibitions of antioxidative enzymes [2, 3]. e various dysfunctions displayed by cells under oxidative stress are due to damages caused by ROS to lipids, proteins, and DNA [4]
Effects of Lead-Induced Heavy Metal Toxicity in Rats. e effects of lead-induced heavy metal toxicity on liver and kidney function biomarkers were investigated by comparing the AST, ALT, GGT, urea, and creatinine levels of the control group and Pb + recovery group (Table 1). ere was a positive significant association (P < 0.05) between the two groups with a recorded R-squared value of more than 95% (Table 1). is indicates that more than 95% of the increase in variation in the ALT, AST, GGT, urea, and creatinine levels may be due to the effect of the administered lead (II) acetate
Summary
Heavy metals are defined as metallic elements that have a relatively high density compared to water. Since density and toxicity are interrelated, heavy metals such as arsenic can induce toxicity at a low level of exposure [1]. Heavy metals are well known for inducing oxidative stress. E mechanisms they apply in inducing oxidative stress include the production of reactive oxygen species (ROS), depletion of intracellular antioxidant stores and free radical scavengers, and inhibitions of antioxidative enzymes [2, 3]. E various dysfunctions displayed by cells under oxidative stress are due to damages caused by ROS to lipids, proteins, and DNA [4]. Human exposure to heavy metals is almost inevitable due to their ubiquitous nature, and some are nonbiodegradable, especially the nonessential heavy metals
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