Abstract
Mercury exposure is a common cause of metal poisoning which is biotransformed to highly toxic metabolites thus eliciting biochemical alterations and oxidative stress. Luteolin, a phenolic compound found in many natural products, has multiple biological functions. Our study was aimed to explore the biological effects of luteolin in a liver injury model induced in rats by mercuric chloride (HgCl2). Criteria for injury included liver enzyme, glutathione and malondialdehyde levels, histopathology, TUNEL assay, hepatocyte viability and reactive oxygen species levels. The results showed that luteolin protected against HgCl2-induced liver injury. Luteolin increased total nuclear factor-erythroid-2-related factor 2 (Nrf2) levels in the presence of HgCl2. Upregulation of its downstream factors, heme oxygenase-1 and NAD(P)H quinone oxidoreductase 1, was also observed. This suggested that protection by luteolin against HgCl2-induced liver injury involved Nrf2 pathway activation. Luteolin also decreased expression of nuclear factor-κB (NF-κB) and P53. HgCl2 exposure led to increased Bcl-associated X protein (Bax), and decreased Bcl-2-related protein long form of Bcl-x (Bcl-xL) and B-cell leukemia/lymphoma-2 (Bcl-2) expression, leading to an increased Bax/Bcl-2 ratio. Taken together, our data suggested that decreasing oxidative stress is a protective mechanism of luteolin against development of HgCl2-induced liver injury, through the Nrf2/NF-κB/P53 signaling pathway in rats.
Highlights
Mercury, in the inorganic form mercuric chloride (HgCl2), is the third most dangerous heavy metal and metalloid element, after arsenic and lead, according to the Agency for Toxic Substance and Disease Registry [1]
Values for erythrocytes, hematocrit and hemoglobin were close to control values in rats administered only luteolin. These parameters were significantly decreased in the HgCl2-treated group, compared with other groups
Compared with the control group, leukocyte counts were significantly increased and platelet counts significantly decreased in the HgCl2-treated group and luteolin administration prevented this change
Summary
In the inorganic form mercuric chloride (HgCl2), is the third most dangerous heavy metal and metalloid element, after arsenic and lead, according to the Agency for Toxic Substance and Disease Registry [1]. Mercury has long been considered a toxic metal, it still has numerous important industrial uses and poisoning from occupational exposure and environmental pollution continues to be a concern [2]. In several in vitro and in vivo studies, damaging effects induced by mercury were related to adverse health impacts including cancer, neurological disorders and cardiovascular diseases [3,4]. Primary murine hepatocytes are frequently used as a model for investigating the toxicity and protective mechanisms associated with various toxins. Based on available experimental data, it is a reasonable hypothesis that mercury toxicity involves oxidative stress, inflammation and apoptosis
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