Benzene Metabolism (Toxicokinetics and the Molecular Aspects of Benzene Toxicity)
Muzaffer Aksoy in Benzene Carcinogenicity, 2017
Determination of benzene metabolism in humans was first evaluated as a measure of exposure. Yant et al.39 suggested that since benzene metabolites in the urine could be detected as ethereal sulfates, it would be possible to estimate benzene exposure by measuring the ratio of inorganic to organic sulfate. Normally the inorganic sulfate is present at about four times the organic levels. Exposure tends to increase the organic sulfate, and lower the inorganic. Hammond and Herman40 suggested that of total sulfates, inorganic sulfates of 80 to 95% were normal, 70 to 80% indicated some exposure to benzene, 60 to 70% suggested a dangerous level of benzene exposure, and 0 to 60% indicated that benzene levels were sufficiently high enough to provide an extremely dangerous atmosphere for humans. In humans, the sulfate is the major conjugate of phenol until levels of approximately 400 mg/l are reached. Beyond that level glucuronides are seen.24,25 Teisinger and Skramovsky41 exposed humans to benzene at 100 ppm for 5 hr and found that the urine contained primarily phenol with small amounts of catechol.
Xenobiotic Biotransformation
Robert G. Meeks, Steadman D. Harrison, Richard J. Bull in Hepatotoxicology, 2020
Arylamine biotransformation provides an additional example of how dose and duration of exposure can influence the degree of toxicity. Sulfation, glucuronidation, and acetylation all result in electrophilic intermediates (Kadlubar and Beland, 1985). The acetylated and glucuronidated conjugates however, are more stable than the sulfated conjugate; therefore, acetylation and glucuronidation are considered detoxifying (Mulder, 1979). Acute exposures tend to lead to conjugation with the sulfate since it is a low-affinity, high-capacity system. As the dose increases, acetylation and glucuronidation tend to predominate since acetylation is an intermediate affinity and capacity system and glucuronidation is a low-affinity, high-capacity system. With chronic exposures, glucuronidation is favored since it is inducible and sulfation and acetylation are not.
Asphyxia
Kevin L. Erskine, Erica J. Armstrong in Water-Related Death Investigation, 2021
Hydrogen sulfide is a gas originating from the natural environment, organic decomposition, and industry. Specific sources include sewers, septic tanks, the manufacture of petroleum-containing products and paper, natural gas, and volcanoes.8 It is commonly described as having a rotten egg odor. At higher concentrations in the ambient environment and with prolonged inhalation, its odor becomes undetectable due to paralysis of the olfactory nerves, and respiratory impairment and unconsciousness may ensue.8 Due to the occupational hazards and past reports of deaths, OSHA regulations restrict the amount of exposure and require training, equipment for detection of the gas, and the use of respiratory protective equipment.13,14 The action of H2S is at the cellular level, similar to cyanide. During the scene investigation, blackening of metal objects, including coins, may be noted. At autopsy, a greenish discoloration of the tissues, in addition to the characteristic odor, may be noted. Prompt toxicological testing may reveal elevated sulfate ion or thiosulfate levels.8
Xenobiotic C-sulfonate derivatives; metabolites or metabonates?
Published in Xenobiotica, 2018
Two mechanisms were proposed for the formation of these sulfonic acid metabolites. Firstly, the attachment via the double bond of the sulfhydryl group of cysteine alone or within reduced glutathione followed by degradation to the thiol and subsequent exhaustive oxidation to the sulfonate. The second was that a sulfate group may be reduced to a sulfite (SO2-3) or bisulfite (hydrogen sulfite; HSO-3) which then reacts to yield the sulfonate conjugate. The reduction of sulfate to sulfite has been shown to occur in the intestine via the action of gut microflora (Robinson, 1965; Schiff & Hodson, 1973) and the addition of bisulfite to an unsaturated bond to form a sulfonate is a well-known reaction in organic chemistry (Heath & Piggot, 1947; Kharasch et al., 1938; Messel, 1871; Redtenbacker, 1848; Tilley, 1848). Indeed, the authors preferred this latter explanation and also reported that the sulfonic acid conjugates could be synthesized readily in the laboratory by stirring flumipropyn in SO2 solution under basic conditions (Yoshino et al., 1993).
Pollution assessment and estimation of the percentages of toxic elements to be removed to make polluted drinking water safe: a case from Nigeria
Published in Toxin Reviews, 2023
Johnbosco C. Egbueri, Daniel A. Ayejoto, Johnson C. Agbasi
Sulfate is naturally found in water as a result of gypsum and other common minerals leaching. The discharge of industrial wastes and home sewage tends to increase the concentration of this substance (Hammarstrom et al.2005, Porowski et al.2019). As seen in Table 1, the values of this parameter in the waters tested in this study area are highly varied. They range from 7.0 to 130 mg/L, with an average of 40.643 mg/L, well below WHO and NIS guidelines of 250 mg/L. The occurrence of a high SO42− concentration is attributable to the rocks that the water passes through. It is suggested that the geology of this area could also comprise of sedimentary deposits such as gypsum (CaSO4). Interestingly, the examined waters meet the NIS (2007) and WHO (2017) benchmark of SO4 concentration of less than 250 mg/L.
In silico prediction of post-translational modifications in therapeutic antibodies
Published in mAbs, 2022
Tyrosine sulfation is an enzymatic modification that is catalyzed by tyrosylprotein sulfotransferases (TPSTs). During sulfation, a sulfate group is attached to the hydroxyl group of tyrosine residues.111 Tyrosine sulfation has been reported for a few monoclonal and bispecific antibodies.111–114 Sulfation of mAbs can occur in Chinese hamster ovary (CHO) cells during the cell culture. The degree of tyrosine sulfation in CHO cells varies due to differential expression of phosphoadenosine-5ʹ-phosphosulfate (PAPS) synthetase and TPST. PAPS synthetase converts ATP to PAPS; TPST transfers the sulfo group from PAPs to tyrosine residues.115 Sulfation in mAbs generates acidic variants,111 but the impact of tyrosine sulfation on the safety and efficacy of therapeutic antibodies has not yet been established.5
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