Toxicity of carbon tetrachloride, free radicals and role of antioxidants

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dc.contributor.authorUnsal, Velid
dc.contributor.authorCicek, Mustafa
dc.contributor.authorSabancilar, Ilhan
dc.date.accessioned2024-04-24T17:18:01Z
dc.date.available2024-04-24T17:18:01Z
dc.date.issued2021
dc.departmentDicle Üniversitesien_US
dc.description.abstractSeveral chemicals, including environmental toxicants and clinically useful drugs, cause severe cellular damage to different organs of our body through metabolic activation to highly reactive substances such as free radicals. Carbon tetrachloride is an organic compound of which chemical formula is CCl4. CCl4 is strong toxic in the kidney, testicle, brain, heart, lung, other tissues, and particularly in the liver. CCl4 is a powerful hepatoxic, nephrotoxic and prooxidant agent which is widely used to induce hepatotoxicity in experimental animals and to create hepatocellular carcinoma, hepatic fibrosis/cirrhosis and liver injury, chemical hepatitis model, renal failure model, and nephrotoxicity model in recent years. The damage-causing mechanism of CCl4 in tissues can be explained as oxidative damage caused by lipid peroxidation which starts after the conversion of CCl4 to free radicals of highly toxic trichloromethyl radicals (center dot CCl3) and trichloromethyl peroxyl radical (center dot CCl3O2) via cytochrome P450 enzyme. Complete disruption of lipids (i.e., peroxidation) is the hallmark of oxidative damage. Free radicals are structures that contain one or more unpaired electrons in atomic or molecular orbitals. These toxic free radicals induce a chain reaction and lipid peroxidation in membrane-like structures rich in phospholipids, such as mitochondria and endoplasmic reticulum. CCl4-induced lipid peroxidation is the cause of oxidative stress, mitochondrial stress, endoplasmic reticulum stress. Free radicals trigger many biological processes, such as apoptosis, necrosis, ferroptosis and autophagy. Recent researches state that the way to reduce or eliminate these CCl4-induced negative effects is the antioxidants originated from natural sources. For normal physiological function, there must be a balance between free radicals and antioxidants. If this balance is in favor of free radicals, various pathological conditions occur. Free radicals play a role in various pathological conditions including Pulmonary disease, ischemia / reperfusion rheumatological diseases, autoimmune disorders, cardiovascular diseases, cancer, kidney diseases, hypertension, eye diseases, neurological disorders, diabetes and aging. Free radicals are antagonized by antioxidants and quenched. Antioxidants do not only remove free radicals, but they also have anti-inflammatory, anti-allergic, antithrombotic, antiviral, and anti-carcinogenic activities. Antioxidants contain high phenol compounds and antioxidants have relatively low side effects compared to synthetic drugs. The antioxidants investigated in CCI4 toxicity are usually antioxidants from plants and are promising because of their rich resources and low side effects. Data were investigated using PubMed, EBSCO, Embase, Web of Science, DOAJ, Scopus and Google Scholar, Carbon tetrachloride, carbon tetrachloride-induced toxicity, oxidative stress, and free radical keywords. This study aims to enlighten the damage-causing mechanism created by free radicals which are produced by CCl4 on tissues/cells and to discuss the role of antioxidants in the prevention of tissue/cell damage. In the future, Antioxidants can be used as a therapeutic strategy to strengthen effective treatment against substances with high toxicity such as CCl4 and increase the antioxidant capacity of cells.en_US
dc.identifier.doi10.1515/reveh-2020-0048
dc.identifier.endpage295en_US
dc.identifier.issn0048-7554
dc.identifier.issn2191-0308
dc.identifier.issue2en_US
dc.identifier.pmid32970608
dc.identifier.scopus2-s2.0-85094100740
dc.identifier.scopusqualityQ1
dc.identifier.startpage279en_US
dc.identifier.urihttps://doi.org/10.1515/reveh-2020-0048
dc.identifier.urihttps://hdl.handle.net/11468/18543
dc.identifier.volume36en_US
dc.identifier.wosWOS:000656354100012
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoenen_US
dc.publisherWalter De Gruyter Gmbhen_US
dc.relation.ispartofReviews on Environmental Health
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAntioxidantsen_US
dc.subjectCarbon Tetrachlorideen_US
dc.subjectHepatotoxicityen_US
dc.subjectNephrotoxicityen_US
dc.subjectNeurotoxicityen_US
dc.subjectOxidative Stressen_US
dc.titleToxicity of carbon tetrachloride, free radicals and role of antioxidantsen_US
dc.titleToxicity of carbon tetrachloride, free radicals and role of antioxidants
dc.typeReview Articleen_US

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