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Solvent Exposure and Toxic Responses
Published in Stephen K. Hall, Joana Chakraborty, Randall J. Ruch, Chemical Exposure and Toxic Responses, 2020
Phenols are aromatic hydrocarbons with one or more hydroxyl groups attached to the benzene ring. The simplest of the compounds is phenol, which contains only one hydroxyl group on a benzene ring. Other examples include cresol (methyl phenol), catechol (1,2-benzenediol), resorcinol (1,3-benzenediol), and hydroquinone (1,4-benzenediol). Phenol is used as a cleaning agent and disinfectant, but its primary use is as a chemical intermediate for resins and pharmaceuticals. Cresol is used primarily as a disinfectant. Catechol is used in photography, fur dying, leather tanning, and as a chemical intermediate. Resorcinol is used as a chemical intermediate for adhesives, dyes, and pharmaceuticals. Hydroquinone is used in photography, as a polymerization inhibitor, and as an antioxidant.
Toxicology
Published in Martin B., S.Z., of Industrial Hygiene, 2018
Phenols are aromatic hydrocarbons with one or more hydroxyl groups attached to the benzene ring. The simplest of the compounds is phenol, which contains only one hydroxyl group on a benzene ring. Other examples include cresol (methyl phenol), catechol (1,2-benzenediol), resorcinol (1,3-benzenediol), and hydroquinone (1,4-benzenediol). Phenol is used as a cleaning agent and disinfectant, but its primary use is as a chemical intermediate for resins and pharmaceuticals. Cresol is used primarily as a disinfectant. Catechol is used in photography, fur dying, leather tanning, and as a chemical intermediate. Resorcinol is used as a chemical intermediate for adhesives, dyes, and pharmaceuticals. Hydroquinone is used in photography, as a polymerization inhibitor, and as an antioxidant.
List of Chemical Substances
Published in T.S.S. Dikshith, and Safety, 2016
Exposures to hydroquinone in large quantities by accidental oral ingestion produce toxicity and poisoning. The symptoms of poisoning include, but are not limited to, blurred speech, tinnitus, tremors, sense of suffocation, vomiting, muscular twitching, headache, convulsions, dyspnea and cyanosis from methemoglobinemia, coma, and collapse from respiratory failure. Occupational workers should be allowed to work with protective clothing and dust masks with full-face or goggles to protect the eyes, and under proper management.
Interaction of L-ascorbic acid and α-tocopherol in alleviating 1, 4-benzoquinone, a metabolite of benzene induced genotoxicity in male Wistar rats
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Ritu Mishra, Karabi Dutta, Manuj Kr. Bharali
Metabolic activation of benzene is necessary to exert its toxic effect and it is mediated through the formation of many intermediates which include phenol, hydroquinone, muconaldehyde and catechol [1]. Bio-activation of benzene takes place primarily in the liver by cytochrome p450 mediated pathway and phenolic compounds (hydroquinone) so formed in the liver are converted to 1,4-benzoquinone (BQ) in the bone marrow through myeloperoxidase mediated pathway [2]. BQ is the most reactive of all the metabolites of benzene that causes severe genotoxicity in the hematopoietic system leading to leukemia and lymphoma [3]. BQ is known to exert its genotoxic effect by inhibiting the activity of topoisomerase II which leads to severe DNA strand breaks and other genotoxic events, thus converting the essential cellular enzyme into a toxin [4]. Further BQ has been reported to cause bone marrow toxicity and hematotoxicity via oxidative stress and further damage to genetic material. The oxidative DNA damage potential of BQ has also been attributed to the formation of reactive oxygen species (ROS) and covalent binding in benzene-induced toxicity [5].
Proton affinity and gas-phase basicity of pyrogallol and phloroglucinol: a computational study
Published in Journal of Coordination Chemistry, 2021
Collin M. Mayhan, Harshita Kumari, Julia M. Maddalena, Gabriel N. Borgmeyer, Carol A. Deakyne
PAs (-Δrx1H298) and GBs (-Δrx1G298) at 298 K were calculated directly using Equation 1 or indirectly using Equation 2. In the latter equation, B1 is either phloroglucinol or pyrogallol and B2 is the reference base: benzene, phenol, catechol, resorcinol, or hydroquinone. We used only the isodesmic form of this equation; that is, bases B1 and B2 are either both carbon protonated or both oxygen protonated. For use in the isodesmic proton transfer reaction, each reference base and its protonated counterpart were re-optimized at the ωB9X-D/aVTZ level of calculation, and the energetics were re-evaluated at the MP2/aVTZ//ωB97X-D/aVTZ level. The starting structures adopted in the re-optimizations of the dihydroxybenzenes were the most stable forms of the acids and bases identified by Bouchoux and coworkers [40]. Given the calculated MP2/aVTZ//ωB97X-D/aVTZ enthalpy data for the bases of interest and the reference bases, PAiso(B1) is then evaluated from Equation 3, where PAexp(B2) is the experimental proton affinity for the given reference base B2 [40, 41].
Insights into the potential mechanism underlying liver dysfunction in male albino rat exposed to gasoline fumes
Published in Egyptian Journal of Basic and Applied Sciences, 2021
Folarin Owagboriaye, Sulaimon Aina, Rasheed Oladunjoye, Titilola Salisu, Adedamola Adenekan, Gabriel Dedeke
Liver is the chief organ that chemically alters all compounds entering the body. Hydrocarbons and other constituents of petroleum and petrochemical products have been reported to be metabolized in the liver to a greater extent [9]. Benzene has to be metabolized to some hepatic metabolites including phenol, catechol and hydroquinone before it can induce its toxic effect [10]. Cytochrome-P450- mediated biotransformation of BTEX increases its toxicity, especially by hepatic CYP2E1 [11] resulting in increase in reactive oxygen species (ROS) production [12]. An imbalance between ROS and antioxidant defenses can lead to oxidative stress, which can alter hepatic function. Oxidative stress-associated pro-inflammatory factors, including xanthine oxidase (XO) may outstrip endogenous protective capability [6,13], further enhancing cellular damage.