78-33-1 Purity
95%
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Specification
This study highlights the significant and potentially detrimental effects of tefluthrin on the gut microbiota of A. mellifera, including altered bacterial composition and metabolic activity. These findings underscore the need for careful assessment of insecticide use to mitigate potential risks to bee health and pollination ecosystems.
Adult bees were exposed to tefluthrin-infused sugar water for ten days, after which gut bacterial DNA was extracted and analyzed using high-throughput sequencing. A total of 20 bacterial species were identified, predominantly from the phyla Proteobacteria and Bacteroidetes. Tefluthrin-treated bees showed a marked decrease in Cyanobacteria abundance (P < 0.05) at the phylum level. On the genus level, the relative abundance of Bartonella and Serratia increased significantly (P < 0.05). Functional predictions based on cluster of orthologous genes indicated metabolic changes in the gut microbiota of tefluthrin-exposed bees. These alterations contrasted with guadipyr-treated bees, which exhibited significant increases in Gilliamella and Frischella abundance but minimal functional metabolic shifts.
Tefluthrin (TEF) is known to disrupt neuromuscular electrical signaling, leading to symptoms such as muscle spasms and seizures. This study explored the mechanisms by which TEF modulates Nav1.4 channels, crucial for skeletal muscle contraction, and its interplay with the intracellular Navβ4 peptide.
Electrophysiological recordings in Nav1.4-expressing CHO-K1 cells demonstrated that TEF induces a hyperpolarizing shift in the activation and inactivation curves of Nav1.4 channels, significantly prolongs inactivation time constants, and enhances resurgent currents at hyperpolarized potentials. These effects were further amplified when Navβ4 peptide was present, suggesting synergistic modulation. Notably, TEF showed greater potency in enhancing resurgent currents and delaying their decay compared to Navβ4 peptide alone.
Molecular docking studies revealed distinct binding sites for TEF and Navβ4 peptide. TEF binds near DI/S6 and DII/S6 regions, exerting significant allosteric effects on the inactivation gate. Navβ4 peptide interacts at domain linkers, modulating gating differently. Despite their distinct binding mechanisms, both compounds independently and synergistically enhance resurgent currents, resulting in membrane hyperexcitability.
Interestingly, with prolonged depolarization, Navβ4 peptide partially counteracted the TEF-induced delay in inactivation and decay of resurgent currents, indicating competitive interactions. This study underscores TEF's capacity to induce skeletal muscle hyperexcitability via Nav1.4 channel modulation and highlights its synergistic effects with Navβ4 peptide. These findings offer insights into TEF-induced neuromuscular toxicity and its potential impact on muscle physiology.
The molecular formula of Tefluthrin is C17H14ClF7O2.
Some synonyms of Tefluthrin include Tefluthrin, Forza, and BIDD:ER0633.
The CAS number of Tefluthrin is 79538-32-2.
The reference does not mention whether Tefluthrin is an acute toxic substance.
The reference does not mention whether Tefluthrin is considered an environmental hazard.
The reference does not provide specific information about the chemical safety of Tefluthrin.
The reference does not provide the IUPAC name of Tefluthrin.
Yes, Tefluthrin is classified as an EPA Pesticide Chemical with the code 128912.
The UNII code of Tefluthrin is 2HE8P42H2J.
The reference does not provide information about the widespread use of Tefluthrin in agriculture.