RESUMEN
Tefluthrin is a Type I pyrethroid insecticide widely used all over the world. Residues of tefluthrin in various agricultural and animal-derived products may be related to potential human health risks. Tefluthrin metabolism in mammals involves hydrolysis of the ester bond to form cyclopropane acid and 4-methylbenzyl alcohol moieties, followed by oxidation. In this review manuscript, we provide crucial information regarding the toxicity of pyrethroids and propose natural antioxidants for amelioration poisoning in humans and animals. We call for the rational use of tefluthrin as an agrochemical product and for greater attention to the residual toxicity caused by tefluthrin in primary and succeeding crops. This greater attention is required given the global use of tefluthrin.
Asunto(s)
Insecticidas , Piretrinas , Animales , Humanos , Ciclopropanos/química , Hidrocarburos Fluorados/química , MamíferosRESUMEN
Growth retardation is a global public health problem that is highly prevalent especially in low-and middle-income countries, which is closely related to the consumption of grains contaminated with T-2 toxin, a risk for human and animal health. However, the possible targets that can relieve T-2 toxin-induced growth retardation still need to be explored. In the present study, T-2 toxin was used as an environmental exposure factor to induce growth retardation and further explore the regulatory role of lncRNA in growth retardation. The present study systematically characterised the expression profiles of lncRNAs and identified a lncRNA lncMST that is related to growth retardation in T-2 toxin-administered rats. Functionally, lncMST could alleviate cell cycle arrest and apoptosis in T-2 toxin-treated GH3 cells. Mechanistically, lncMST, serve as an inducible chaperone RNA, involved in the paradigm "Chemical-induced stress related growth retardation", through recruiting the EPRS/HSP90AB1 complex to increase HDAC6 expression, thus further alleviating T-2 toxin-induced growth retardation. These findings for the first time demonstrate that the probable therapeutic relationship between lncMST and growth retardation, providing an explanation and therapeutic targets for the pathogenesis of growth retardation.