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Hazard Characterization and Dose–Response Assessment
Published in Ted W. Simon, Environmental Risk Assessment, 2019
Dose addition assumes a common mode of action, and if the MOA is not known, EPA recommends separating chemicals by the affected target organ. This recommendation falls short: hydrogen sulfide and cyanide both form methemoglobin adducts, and both prevent oxygen transport by red blood cells. Does this respiratory inhibition represent a common mode of action? Hydrogen sulfide is detoxified by sulfide oxidase, an enzyme that produces thiosulfate from hydrogen sulfide. Cyanide is detoxified by rhodanese, an enzyme that uses thiosulfate to convert cyanide to thiocyanate, which is also found in cruciferous vegetables like broccoli. The increased levels of thiosulfate accelerate detoxification of cyanide. Cyanide antidote kits used by poison control centers contain injectable thiosulfate, and here is an instance where two chemicals with a common MOA fail to be dose-additive and act as antagonists as defined below.24
Biodegradation of cyanide in cassava wastewater using a novel thermodynamically-stable immobilized rhodanese
Published in Preparative Biochemistry & Biotechnology, 2021
Adedeji Nelson Ademakinwa, Mayowa Oladele Agunbiade, Oladapo Fagbohun
For the submerged fermentation for the production of rhodanese, cyanide was the sole nitrogen source. The medium consisted of the following as described by Ray et al.:[14] Starch (0.03 M) NaCl (17 µM); CaCl2 (90 µM); MgSO4. 7H2O (1.6 mM); K2HPO4.2H2O (1.4 mM); KCN (4.0 mM) and glucose (10 mM); the medium was filtered, pH adjusted to 6.0, sterilized by autoclaving at (121 °C; 15 psi) and cooled to 25 °C. Agar plugs (8 mm) cut from the actively-growing regions of the fungus on MEA in Petri-dishes were used to inoculate the medium. The inoculated medium was incubated for 5 days and aliquots (5 mL) were withdrawn each day, centrifuged at 4000×g for 5 min. The supernatant served as the extracellular rhodanese while the mycelia collected after centrifugation was homogenized in 0.5 mM phosphate buffer pH 6.0 using acid-washed sand (for cell disruption).[28] The slurry collected was further centrifuged at 13,500×g at 4 °C for 20 min. The resulting supernatant served as the source of intracellular rhodanese.[21]
Physiological and pathophysiological implications of hydrogen sulfide: a persuasion to change the fate of the dangerous molecule
Published in Journal of the Chinese Advanced Materials Society, 2018
Jan Mohammad Mir, Ram Charitra Maurya
The further extension of chemical and biochemical catabolic destiny of H2S and many more other aspects are probably yet to be explored.[53] For instance, the formation of sulfhemoglobin by H2S from methemoglobin might act as a metabolic sink for H2S. In addition to it, H2S gets rapidly oxidized to thiosulfate (S2O32-) by mitochondria and is subsequently converted to sulfite (SO32-) and sulfate (SO42-). Another chemical feature of H2S is the methylation by thiol-S-methyltransferase to yield methanethiol (CH3SH) and dimethylsulfide (CH3SCH3), and it is also a substrate (especially in the colon) for rhodanese (thiosulfate: cyanide sulfurtransferase), leading to the formation of SCN- and SO42-. Despite these catabolic characteristics, H2S is a strong reducing agent and is likely to be consumed by endogenous oxidant species in the vasculature,[54–56] viz., peroxynitrite, superoxide, and hydrogen peroxide.
Physiologically based pharmacokinetic modeling of hydrogen cyanide in humans following the oral administration of potassium cyanide and cyanogenic glycosides from food
Published in Human and Ecological Risk Assessment: An International Journal, 2020
Quoc Ba Tran, Tanapon Phenrat, Manupat Lohitnavy
The amount of cyanide metabolized to HCN via the rhodanese pathway () was calculated using the equation by Michaelis Menten: where Km is the binding affinity of rhodanese (μmol/l), CLi is the concentration of cyanide in the liver (μg/l), and Vmax is the maximum velocity of rhodanese (μmol/h).