Effects of pyriproxyfen on zebrafish brain mitochondria and acetylcholinesterase

Pesticide Pollution: Detrimental Outcomes and Possible Mechanisms of Fish Exposure to Common Organophosphates and Triazines

“…Mitochondria generate a lot of free radicals, which contribute to a lot of pathological and degenerative changes, particularly when an organism is being affected by chemical stressors. After being exposed to pyriproxyfen (0.001-10 µmol•L −1 for 16 h), male zebrafish showed a significant decrease in complex I/II respiratory control and Ca 2+ uptake capability in brain tissue, as well as a significant increase in O 2 radical dots revealed by the MitoSOX test [169]. A noticeable mitochondrial impairment in Ca 2+ release could be linked to a decrease of mitochondrial membrane potential or pesticide-induced endoplasmic reticulum damage.…”

“…Fish or cell toxicity, on the other hand, is unrelated to mitochondrial toxicity, implying that few chemicals have the same harmful mechanism and a huge portion of them have none [167]. In general, different classes of pesticides share relatively the same features of mitochondrial toxicity, among them significant swelling in mitochondria, low cytoplasm/mitochondria ratio, less dense matrix and vacuolated mitochondria with matrix disoriented cristae in histosections, a decrease in NADH cytochrome C reductase and succinate cytochrome C reductase in the mitochondrial respiratory chain, uncoupling of mitochondrial oxidative phosphorylation, and a decrease in mitochondrial transmembrane potential [168][169][170]. It is worth noting that there is a paucity of data on mitochondrial toxicity as a response to triazine pesticide exposure in fish, but studies on mammalian models suggest the same mechanism of mitochondrial toxicity observed for other pesticide classes.…”

Systematic Review of Calcium Channels and Intracellular Calcium Signaling: Relevance to Pesticide Neurotoxicity

“…The ER has been shown to be the predominant Ca 2+ reservoir in malathion-and TBI-induced Ca 2+ release in human astrocyte cultures [44,45]. The results of both in vitro studies suggest that the release of Ca 2+ stored in the ER might be the main mechanism by which these pesticides increase [Ca 2+ ]i. Pyriproxyfen (0.1 µg/mL) ↓ Ca 2+ uptake by up to 50% Pyridoxyphene (0.01 or 0.1 µg/mL) ↓ mitochondrial Ca 2+ release by approximately 80% [110] Abbreviations: GHA, Gibco ® human astrocytes; SERCA, sarco(endo)plasmic reticulum Ca 2+ -ATPase; LCT, lambda-cyhalothrin; IP 3 , inositol 1,4,5-trisphosphate.…”

“…Specifically, the findings of the in vivo study by Kaur et al [109] demonstrate that chronic exposure of Wistar rats to dichlorvos (6 mg/kg) significantly increased Ca 2+ uptake by the mitochondria, while the team of Azevedo et al [110] found that in the presence of pyriproxyfen (0.01 or 0.1 µg/mL), the mitochondrial Ca 2+ release was markedly reduced in zebrafish. However, Azevedo et al [110] also observed that the higher concentration of pyriproxyfen (0.1 µg/mL) reduced the Ca 2+ uptake into the cell interior, which could be related to a loss of mitochondrial membrane potential, or a damage of the ER caused by the pesticide. These results are in line with the extensive evidence pointing to the mitochondria as one of the targets of neurotoxic action exerted by pesticides [116][117][118][119].…”

Synthesis of Esters Containing Cinnamoyl Motif with Potential Larvicide Action: A Computational, Ecotoxicity and in Vitro Cytotoxicity Assessments

“…For this, there are essentially three monitoring methods: mechanical, biological, and chemical, the last being the major current means of disease control [11] . Among synthetic insecticides, temephos and pyriproxyfen are highlighted, nevertheless, the mosquito has been displaying resistance to these insecticides and toxic effects have been reported both in animals and crustaceans [12,13] …”