Most of the compounds have physiologically active properties, and their biological properties are often attributed to the heteroatoms contained in their molecules, and most of these heteroatoms also appear in cyclic structures. A Journal, Article, Research Support, Non-U.S. Gov’t, Toxicology called The selective neurotoxicity produced by 3-chloropropanediol in the rat is not a result of energy deprivation, Author is Skamarauskas, J.; Carter, W.; Fowler, M.; Madjd, A.; Lister, T.; Mavroudis, G.; Ray, D. E., which mentions a compound: 60827-45-4, SMILESS is OC[C@H](O)CCl, Molecular C3H7ClO2, Computed Properties of C3H7ClO2.
The biochem. mechanism of toxicity of the exptl. astrocyte neurotoxicant and food contaminant S-3-chloro-1,2-propanediol (3-CPD) has been proposed to be via inhibition of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). We have confirmed this action in liver, which shows inhibition to 6.0±0.7% control at the neuropathic dose of 140 mg/kg. However, GAPDH activity in brain only fell to a min. of 54±24% control, and the concentrations of lactate and pyruvate (the downstream products of GAPDH), showed no pre-neuropathic decreases in 3-CPD susceptible brain tissue. There was no inhibition of GAPDH activity in primary astrocyte cultures at sub-cytotoxic exposures. We therefore sought alternative mechanisms to explain its toxicity to astrocytes. We were able to show that 3-CPD is a substrate for glutathione-S-transferase and also that, after bioactivation by alc. dehydrogenase, it generates an irreversible inhibitor of glutathione reductase. In addition, incubation of brain slices from the 3-CPD-vulnerable inferior colliculus produces a depletion of glutathione and an inhibition of glutathione-S-transferase that is not seen in equivalent slices taken from the 3-CPD-resistant occipital neocortex. A smaller but significant and similarly regionally selective decrease in glutathione content is also seen in vivo. We conclude that 3-CPD does not produce its astrocytic toxicity via energy deprivation, and suggest that selective bioactivation and consequent disruption of redox state is a more likely mechanism.
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Reference:
Iodide – Wikipedia,
Iodide – an overview | ScienceDirect Topics – ScienceDirect.com