Effects of chlorpyrifos on early development and anti-predator behavior of agile frogs

The widespread application of pesticides makes it important to understand the impacts of these chemicals on wildlife populations. Chlorpyrifos is an organophosphate insecticide which can affect the development and behavior of aquatic organisms and may thereby alter predator-prey interactions. To investigate how environmentally relevant, sublethal concentrations of chlorpyrifos affect anti-predator behavior and larval development of the agile frog (Rana dalmatina), we exposed tadpoles to one of three concentrations (0, 0.5 and 5 μg chlorpyrifos / L) either for a brief period of three days (acute exposure) or throughout larval development (chronic exposure). We observed tadpole activity and space use in the presence or absence of chemical cues of predatory fish. We also assessed mortality, time to metamorphosis, mass at metamorphosis, brain morphology and sex ratio. We found that tadpoles chronically exposed to 5 μg/L chlorpyrifos swam distances that were longer by more than 20 % and exhibited body masses at metamorphosis that were lower by ca. 7 % than in control individuals, but the other fitness-related traits remained unaffected. The lower concentration of chlorpyrifos applied chronically, and either one of the acute chlorpyrifos treatments did not influence any measured trait. Our results demonstrate that exposure to chlorpyrifos can induce changes in locomotor activity and may result in lowered body mass of agile frog tadpoles, but only if the insecticide is present chronically at concentrations which are rarely reached in natural waterbodies. Thus, agile frog tadpoles appear to be relatively tolerant to chlorpyrifos, but may nonetheless suffer from its presence in situations of repeated high-dose application.

Oxidative Stress and Calcium Dyshomeostasis Mediated CPF-Induces EPC Cell Apoptosis and Necroptosis

Chlorpyrifos (CPF) is a broadly used organophosphate insecticide, and as environmental contamination has been confirmed to be harmful to the health of humans and animals, the effects of CPF on fish are still unclear. We aim to detect whether CPF has effects on the common carps, and identify the mechanisms of the effects. In accordance with the IC50 of CPF for epithelioma papulosum cyprini (EPC) cells was 8.945 µM, 0, 3, 5 and 7 µM CPF were marked as C, L, M and H group. The results indicated that CPF exposure led to oxidative stress in EPC cells. Moreover, Calcium ion (Ca2+) imaging indicated that CPF triggers Ca2+ dyshomeostasis, as induced ER Ca2+ fluxed into cytoplasm and mitochondrial, and mediates endoplasmic reticulum (ER) stress and mitochondrial Ca2+ overload, which have further confirmed with the increased transcription of ER stress related genes. Meanwhile, CPF induced collapse of mitochondrial membrane potential (MMP), enhancement of ROS generation and depletion of ATP level in both cytoplasm and mitochondrial, substantiated mitochondrial dysfunction has been evoked. Besides, the AO/EB staining and flow cytometry analysis ascertained that CPF induces apoptosis and necroptosis in EPC cells. Hence, we further verified that via determining the expression of apoptotic pathway genes and necroptotic pathway genes. Consequently, we illuminated the mechanisms of CPF effects on the common carps from the perspective of Ca2+ homeostasis, and provided a novel concept for investigating the toxicity of CPF as environmental pollution on aquatic organisms.

The pesticide chlorpyrifos promotes obesity by inhibiting diet-induced thermogenesis in brown adipose tissue

Obesity results from a caloric imbalance between energy intake, absorption and expenditure. In both rodents and humans, diet-induced thermogenesis contributes to energy expenditure and involves the activation of brown adipose tissue (BAT). We hypothesize that environmental toxicants commonly used as food additives or pesticides might reduce BAT thermogenesis through suppression of uncoupling protein 1 (UCP1) and this may contribute to the development of obesity. Using a step-wise screening approach, we discover that the organophosphate insecticide chlorpyrifos suppresses UCP1 and mitochondrial respiration in BAT at concentrations as low as 1 pM. In mice housed at thermoneutrality and fed a high-fat diet, chlorpyrifos impairs BAT mitochondrial function and diet-induced thermogenesis, promoting greater obesity, non-alcoholic fatty liver disease (NAFLD) and insulin resistance. This is associated with reductions in cAMP; activation of p38MAPK and AMPK; protein kinases critical for maintaining UCP1 and mitophagy, respectively in BAT. These data indicate that the commonly used pesticide chlorpyrifos, suppresses diet-induced thermogenesis and the activation of BAT, suggesting its use may contribute to the obesity epidemic.

Electrochemical Detection of Fenthion Insecticide in Olive Oils by a Sensitive Non-Enzymatic Biomimetic Sensor Enhanced with Metal Nanoparticles

Fenthion, an organophosphate insecticide, is a cholinesterase inhibitor and is highly toxic. An electrochemical sensor based on molecularly imprinted polymer is developed here for its detection. For this purpose, 2-aminothiophenol mixed with gold nanoparticles was immobilized on screen-printed gold electrodes. The FEN pattern was then fixed before being covered with 2-aminothiophenol. Cyclic voltammetry, differential pulse voltammetry and electrochemical impedance spectroscopy methods were used for the electrochemical characterization. The low detection limit was 0.05 mg/Kg over a range of 0.01–17.3 µg/mL. The sensor was successfully applied for the determination of FEN in olive oil samples with high recovery values.

Atropine Induced Psychosis in Organophosphate Insecticide Poisoning and it's Management: A case series

Atropine is an established antidote in organophosphorus poisoning. It is an anticholinergic that inhibits the muscarinic actions of acetylcholine at postganglionic parasympathetic neuroeffector sites including secretory glands, smooth muscle, and CNS sites. In the literature, the cases of atropine intoxication are not uncommon. We report a case series of five cases of atropine induced psychotic disorder in patients, who manifested with delirium, hallucinations, nervousness, drowsiness, weakness, irrelevant talk, flushing along with tachycardia, and non-reactive dilated pupils suggesting possible anti-cholinergic abuse. The patients reported at the Department of Medicine-Unit II, Sheikh Zayed Medical College/Hospital, Rahim Yar Khan, from January to June 2019. The patients were managed symptomatically by titrating down the atropine's dose, administration of benzodiazepine, and antipsychotics.