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Pathological Manifestations and Mechanisms of Metal Toxicity
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
The liver has an important role in metal metabolism, biotransformation, and elimination; therefore it is fundamental in the response to metal toxicity and potential for metal bioaccumulation. The liver is also a critical organ for metal detoxification, predominately through the induction of metalloproteins such as metallothionein (MT), transferrin, and ceruloplasmin (Wolff, Lee, Abouhamed, & Thevenod, 2008). Disruption of hepatic detoxification processes or excessive metal intake leads invariably to the development of liver injury. Acute liver lesions, frequently observed as hepatocyte necrosis, are usually the result of exposure to high metal doses in a short period of time and can, non-uncommonly, be associated with death. Chronic liver injury is a continuum of ongoing inflammatory insult that is accompanied by increased connective tissue (fibrosis) that, depending on severity and persistence of metal exposure, can lead to cirrhosis and in some cases can ultimately be associated with liver cancer.
Terpenoids in Treatment of Liver Disease
Published in Dijendra Nath Roy, Terpenoids Against Human Diseases, 2019
Sujan Chatterjee, Debajyoti Patra, Pujita Ghosh, Akash Prasad, Kaustav Dutta Chowdhury
Perillyl alcohol—4-(prop-1-en-2-yl) cyclohex-1-en-1-yl—is a monocyclic monoterpene derived via the MVA pathway in plants. Perillyl alcohol is a constituent of caraway, lavender and lilac oils, cherries, cranberries, sage, spearmint, peppermint, celery seeds and certain other plants (Chen et al. 2015). Perillyl alcohol can be used effectively in treatment of liver injury (Khan et al. 2011). Oxidative stress and inflammation are two major etiological factors that are suggested to play key roles in the development of ethanol-induced liver injury (Khan et al. 2011). The release of pro-inflammatory cytokines like TNF-α and the activation of NF-κB may strongly intensify inflammation and cell damage. Additionally, ROSs also exert significant effect in this whole-cell signalling machinery. Khan et al. (2011) successfully demonstrated that pre-treatment with POH, besides exerting an anti-oxidant activity, might be able to modulate TNF-α release and NF-κB activation in the Wistar rat. Serum aspartate aminotransferase (AST), ALT and LDH and hepatic TBARS were increased significantly by ethanol exposure. Ethanol administration decreased hepatic GSH content and the activity of various anti-oxidant enzymes. In addition, TNF-α production and NF-κB activation were increased after ethanol administration. POH pre-treatment significantly ameliorated ethanol-induced acute liver injury, possibly via inhibition of lipid peroxidation, replenishment of the endogenous enzymatic and non-enzymatic defence systems, and down-regulation of TNF-α and NF-κB (Khan et al. 2011).
Pesticides and Chronic Diseases
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 4, 2017
William J. Rea, Kalpana D. Patel
Trivalent arsenicals (or, more likely an arsenious acid metabolite) bind efficiently to the functional thiol groups of many tissue components, including enzymes. Its affinity for thiol groups in keratin accounts for the accumulation of arsenic in skin, nails, and hair in cases of chronic poisoning. When absorbed across the gut wall, these arsenicals injure the splanchnic vasculature, causing abdominal pain, colic, and diarrhea. Once absorbed into the blood, they cause toxic damage to the liver, kidneys, brain, bone marrow (BM), and peripheral nerves. Liver injury is manifest as hepatomegaly, jaundice, and an increase in circulating hepatocellular enzymes LDH and GOT. Renal damage is reflected in albuminuria, hematuria, pyuria, cylinduria, and then azotemia. Acute tubular necrosis may occur in severe poisoning. Injury to blood-forming tissues can take the form of agranulocytosis, aplastic anemia, thrombocytopenia, or pancytopenia. Toxic encephalopathy may manifest as speech and behavioral disturbances. Peripheral neuropathy occurs in both acute and chronic forms.
The role of thioredoxin and glutathione systems in arsenic-induced liver injury in rats under glutathione depletion
Published in International Journal of Environmental Health Research, 2022
Yuanyuan Li, Kun Liang, Lin Yuan, Jing Gao, Linquan Wei, Lijun Zhao
Previous studies have reported arsenic-induced liver injury with increased liver weight and biomarkers and exacerbated liver histology (Santra et al. 1999; Jomova et al. 2011; Gora et al. 2014; Lu et al. 2019). Similarly, our investigation has reconfirmed it and discovered some new aspects of arsenic-related toxicity, like increased liver weight and liver-to-body ratio. Also, higher levels of liver biomarkers such as AST and ALT were observed, similar to the previous reports. In our research, liver injury affects protein synthesis. It causes overproduction of serum ALB in the arsenic group, particularly TP concentrations. Compared with the control, the serum level of ALB and TP in LA, HA, and HABSO was increased, which may be a compensatory effect of liver enlargement. As an essential antioxidant, GSH could protect the body against ROS and play a vital role in liver cell absorption, metabolism, and excretion of arsenic. Conversely, the lack of GSH could diminish the body’s antioxidant impact and affect the body’s metabolism and detoxification of arsenic (Renu et al. 2020; Liu et al. 2022). It was evident that the liver exposed to HABSO exhibited severe damage. An elevated level of arsenic was observed in the serum, liver, and urine. Furthermore, altered liver histopathology and liver architecture were observed, a typical sign of liver injury. The altered morphological and histopathological changes were confirmed using a transmission electron microscope. Our findings showed that the combined effects of arsenic and BSO aggravate liver injury.
An experimental and theoretical study of ROS scavenging by organosulfur compounds from garlic: In silico analysis of metabolic pathways and interactions on CYP2E1
Published in Journal of Sulfur Chemistry, 2022
Mario Guillermo Diaz, Gabriela Veronica Ferrari, Matías Fernando Andrada, Esteban Vega-Hissi, Maria Paulina Montaña, Juan Ceferino Garro Martinez
On the other hand, studies that indicate that some OSC have an inhibitory effect on enzyme members of the cytochrome P450 family, especially the CYP2E1 [17]. This enzyme is capable of metabolizing and activating many substrates, including ethanol, into more reactive and toxic products, contributing to alcohol-induced liver injury. In addition, levels of this enzyme are also elevated in various pathophysiological conditions, such as non-steatohepatitis, diabetes, obesity, cancer, Parkinson and oxidative stress, being an efficient generator of ROS [18–21]. The ROS that can be generated are superoxide anion radical (O2• -) and hydrogen peroxide (H2O2), and in the presence of ferric catalysts produce powerful oxidants, such as the hydroxyl radical (HO·) and the 1-hydroxyethyl radical [22].
A review of the toxicology of oil in vertebrates: what we have learned following the Deepwater Horizon oil spill
Published in Journal of Toxicology and Environmental Health, Part B, 2021
Ryan Takeshita, Steven J. Bursian, Kathleen M. Colegrove, Tracy K. Collier, Kristina Deak, Karen M. Dean, Sylvain De Guise, Lisa M. DiPinto, Cornelis J. Elferink, Andrew J. Esbaugh, Robert J. Griffitt, Martin Grosell, Kendal E. Harr, John P. Incardona, Richard K. Kwok, Joshua Lipton, Carys L. Mitchelmore, Jeffrey M. Morris, Edward S. Peters, Aaron P. Roberts, Teresa K. Rowles, Jennifer A. Rusiecki, Lori H. Schwacke, Cynthia R. Smith, Dana L. Wetzel, Michael H. Ziccardi, Ailsa J. Hall
As the site of detoxification, the liver is often damaged by exposure to pollutants, including oil. Liver injury covers a wide range of effects including hepatic necrosis, lipid accumulation (steatosis), or hepatobiliary dysfunction.