Thiol antidotes effect on lipid peroxidation in mercury-poisoned rats
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Ellagic acid: Pharmacological activities and molecular mechanisms involved in liver protection
2015, Pharmacological ResearchCitation Excerpt :Hg is a toxic and hazardous metal that may exist in the environment [180,181]. Exposure to mercurial compounds induces hepatotoxicity associated with oxidative stress [182–185], generating hepatocellular defects like hepatomegaly, centrilobular hepatic steatosis [186,187], decrease in the synthesis of hepatic coagulation factors [188–192] and diminution in the activity of metabolic enzymes [193]. EA reduces mercuric chloride damage, avoiding the generation of oxidative stress and diminishing the possibility of damage to liver cells [194,195].
Protective effect of curcumin against heavy metals-induced liver damage
2014, Food and Chemical ToxicologyCitation Excerpt :However, it remains unclear whether curcumin can activate Nrf2/Keap1/ARE pathway in models of hepatotoxicity caused by lead poisoning. Hepatocellular effects described for mercury are elevated serum ALT, ornithine carbamyltransferase and serum bilirubin levels, hepatomegaly and centrilobular hepatic steatosis, decrease in the synthesis of hepatic coagulation factors (Kanluen and Gottlieb, 1991; Ashour et al., 1993; Joshi et al., 2011, 2012; Cao et al., 2012), decreased activity of metabolic enzymes (Chang et al., 1973), increase in lipid peroxidation products (Stacey and Kappus, 1982; Benov et al., 1990; Huang et al., 1996; Lin et al., 1996), mitochondrial dysfunction (Belyaeva et al., 2011), proliferation of the endoplasmic reticulum, floccular degeneration of the hepatic mitochondria with extrusion of degenerated hepatic organelles and cytoplasmic debris into the sinusoidal space and engulfed by Kupffer cells and vacuolar degeneration of the mitochondria in the Kupffer cells (Chang and Yamaguchi, 1974; Desnoyers and Chang, 1975a,b). Exposure to mercury compounds induces oxidative stress (Atchison and Hare, 1994; Mahboob et al., 2001; Gutierrez et al., 2006; Al-azzawie et al., 2013; Farina et al., 2013).
N-acetyl cysteine and selenium protects mercuric chloride-induced oxidative stress and antioxidant defense system in liver and kidney of rats: A histopathological approach
2014, Journal of Trace Elements in Medicine and BiologyCitation Excerpt :Mercury is a transition metal and it promotes the formation of reactive oxygen species (ROS) such as superoxide and hydrogen peroxides, which induce oxidative stress, resulting in cell membrane damage [26,27]. Its exposure has also been demonstrated to induce lipid peroxidation by increased thiobarbituric acid reactive substances (TBARS) in liver, kidney, brain and other tissues [28]. In the current study, mercury toxicity was evidenced by determination of liver and kidney function tests, markers of oxidative stress by estimation of LPO level, GSH content, SOD and catalase enzymes activities, mercury ion concentration and histopathological observations of liver and kidney.
Arsenic-induced oxidative stress and its reversibility
2011, Free Radical Biology and MedicineCitation Excerpt :Chelating agents are organic compounds capable of linking together metal ions to form complex ring-like structures called chelates. Sodium 2,3-dimercaptopropane 1-sulfonate (DMPS), DMSA (Scheme 7), and one of its analogues, monoisoamyl-DMSA (MiADMSA), are effective chelators, and the dithiol group in their moieties acts as an oxygen radical scavenger, which helps in inhibiting lipid peroxidation [377–380]. DMSA and DMPS are effective in reversing arsenic-induced toxicity based on enhanced urinary arsenic excretion and restoration of inhibited blood ALAD activity and hepatic glutathione [191,381].
Inhibition of hepatic δ-aminolevulinate dehydratase activity induced by mercuric chloride is potentiated by N-acetylcysteine in vitro
2011, Food and Chemical ToxicologyCitation Excerpt :These lipid peroxides and hydroxyl radical may cause the cell membrane damage and thus destroy the cell. Inorganic mercury also inhibits the activities of the free radical quenching enzymes catalase, superoxide dismutase and glutathione peroxidase (Benov et al., 1990). δ-Aminolevulinate dehydratase (δ-ALA-D; EC 4.2.1.24) is very sensitive to agents which oxidizing sulfhydryl groups, including mercury (Emanuelli et al., 1996).