China
Africa
Explore chapters and articles related to this topic
Perfluorooctanoic acid (PFOA)
Published in Mark S. Johnson, Michael J. Quinn, Marc A. Williams, Allison M. Narizzano, Understanding Risk to Wildlife from Exposures to Per- and Polyfluorinated Alkyl Substances (PFAS), 2021
Exposure of male rats to 1,000 ppm PFOA in the diet induced marked increases in the activity of liver peroxisomal beta-oxidation pathways and carnitine acetyltransferase at both two and 26 weeks of treatment (Uy-Yu et al. 1990a). Female rats showed only slight responses, with the activity of palmitoyl CoA oxidase being significantly induced only after 26 weeks of PFOA treatment, when compared with age-matched female control rats. In addition, carnitine acetyltransferase activity was increased (compared with the control rats) in female rats at both two and 26 weeks of PFOA treatment, yet the activities of both palmitoyl CoA oxidase and carnitine acetyltransferase were significantly lower in PFOA-treated female rats than in PFOA-treated male rats (Uy-Yu et al. 1990a).
Molecular toxicology and carcinogenesis of fumonisins: a review
Published in Journal of Environmental Science and Health, Part C, 2020
Ruth Nabwire Wangia-Dixon, Kizito Nishimwe
The mechanism of fumonisin B1 toxicity is summarized in Figure 5. Sphinganine (Sa) and sphingosine (So) are synthesized de novo from palmitoyl-COA and serine substrates through a myriad of different enzymes including serine palmitoyl transferase, 3-ketoreductase, ceramide synthase and desaturase.48,49 Due to structural similarity between fumonisins and the long chain sphingolipid backbones, fumonisin B1 has the ability to compete with sphingolipids to bind and inhibit ceramide synthases.48–50 Moreover, the ability of ceramide synthase to recognize amine and tricarboxylic acid chain groups favors binding to fumonisin B1. Inhibition of the enzyme ceramide synthase interferes with the sphingolipid metabolism causing free sphingolipid bases and their 1-phosphates to accumulate in cells.51–53 Since ceramide is a precursor to more complex sphingolipids, the loss of de novo ceramide synthesis triggered by fumonisin B1 would result in a decreased pool of these sphingolipids, which play important roles in cell membrane integrity.13,41 The primary mechanism of fumonisins toxicity is thereby established to be disruption of sphingolipid synthesis de novo by way of fumonisin B1 ’s inhibitive action of the enzyme ceramide synthase.11,13,28