Acute Silver Catfish (Rhamdia quelen) Exposure to Chlorantraniliprole Insecticide.

The aim of the current study is to investigate whether silver catfish (Rhamdia quelen) individuals exposed to commercial formulation of the chlorantraniliprole insecticide used in rice crops present changes in biochemical parameters. Fifty-four (54) silver catfish individuals were distributed in six units per tank (n = 6/repetition; triplicate/treatment) and subjected to the following treatments: T1-control, without insecticide; T2 (0.02 µg/L of insecticide) and T3 (0.20 µg/L of insecticide). Exposure time lasted 24 or 96 h, and it was followed by 96 h recovery in pesticide-free water. Results have indicated biochemical changes in cortisol, glucose, lactate and plasma protein levels, as well as few ionic changes in animals' gills during the exposure and recovery periods. Chlorantraniliprole incidence in water resulted in some biochemical changes in silver catfish specimens' plasma and gills throughout the acute exposure protocol (sub-lethal dose). Thus, chlorantraniliprole insecticide has caused osmoregulatory and/or biochemical imbalance in the investigated species under the herein adopted laboratory conditions; these changes did not get back to normal levels even after specimens were left to recover for 96 h in clean water.

Toxicological response of silver catfish (Rhamdia quelen) after acute exposure to a commercial insecticide containing thiamethoxam.

This study assessed the hematological, enzymatic and osmoregulatory responses of silver catfish (Rhamdia quelen) exposed to sublethal concentrations (1.125 and 3.750 µg/L) of a commercial thiamethoxam-containing insecticide used on rice crops. Groups of 6 fish per tank (in triplicate, n = 3, total 54 fish) were exposed for up to 96 h to different concentrations of the compound. After this period, fish were placed in clean water for 48 h. Two fish from each tank (6 per treatment) that had been exposed to the insecticide for 24 h were anesthetized with eugenol and blood was collected to evaluate hematological and biochemical parameters. Blood, liver and muscle were collected for determination of metabolic parameters, plasma cortisol, Cl-, Na+ and K+ levels and H+-ATPase and Na+/K+-ATPase activity in the gill. H+-ATPase activity was higher in fish exposed to 1.125 µg/L insecticide at 24 h compared to control (0.0 µg/L). Differences in cortisol levels were evidenced throughout the experimental period. These results indicated that exposure to the insecticide changed the hematological, biochemical and metabolic profile of the animals, suggesting concern about environmental safety. Therefore, we discourage the use of this pesticide in areas that come into contact with water bodies inhabited by fish.

Purinergic signaling as potential target of thiamethoxam-induced neurotoxicity using silver catfish (Rhamdia quelen) as experimental model.

Thiamethoxam is a broad-spectrum pesticide widely used in agricultural practice throughout the world. Worryingly, this pesticide is considered a potential contaminant on the surface and underground water, being a significant risk to aquatic ecosystems and humans. In this sense, we decided to evaluate the activity of enzymes belonging to purinergic system, which is linked with regulation of extracellular nucleotides and nucleosides, as adenosine triphosphate (ATP) and adenosine (Ado) molecules involved in the regulation of immune and inflammatory responses. Such as the neurotoxic effects of thiamethoxam remain poorly understood, the aim of this study was to evaluate whether purinergic signaling may be considered a potential target of thiamethoxam-induced neurotoxicity in silver catfish (Rhamdia quelen). Brain ectonucleoside triphosphate diphosphohydrolase (ATP as substrate) and 5'-nucleotidases activities were inhibited at 3.75 µg L-1 after 24 h of exposure and at 1.125 and 3.75 µg L-1 after 96 h of exposure compared with the control group. On the other hand, brain adenosine deaminase activity was stimulated at 3.75 µg L-1 after 24 h of exposure and at 1.125 and 3.75 µg L-1 after 96 h of exposure compared with the control group. Brain ATP levels increased at 3.75 µg L-1 after 24 h of exposure and at 1.125 and 3.75 µg L-1 after 96 h of exposure compared with the control group, while the Ado levels decreased. The enzymatic activity of the purinergic signaling did not return to control levels after a 48-h recovery period, revealing the potential neurotoxic effects of thiamethoxam. In summary, the brain purinergic signaling may be considered a potential target for thiamethoxam-induced neurotoxicity in silver catfish.

Imazapyr+imazapic herbicide determines acute toxicity in silver catfish Rhamdia quelen.

Imazapyr (IMY) and imazapic (IMI) are imidazolinone herbicides which have been associated in a commercial formulation (Kifix(®)). To date, there are no studies on the toxicity of an IMY+IMI herbicide in fish. This work aimed to assess the acute toxicity (24 and 96 h) of IMY+IMI (0, 0.488 and 4.88 µg/L) towards Rhamdia quelen through hematological, biochemical, immunological, ionoregulatory and enzymatic indexes. Red blood cell count was lower at 4.88 than at 0.488 µg/L (24 and 96 h); mean corpuscular volume was lower than control at both concentrations (24 h) and at 0.488 µg/L (96 h); lymphocytes declined at 4.88 µg/L comparing to control (96 h); and monocytes increased at 4.88 µg/L (96 h) in comparison with the respective control and with 4.88 µg/L at 24h. Aspartate aminotransferase was higher at 0.488 µg/L (96 h) than the respective control and the respective concentration at 24 h; uric acid reduced at 4.88 µg/L comparing with 0.488 µg/L (96 h); and cortisol was lower at 4.88 µg/L compared to 0.488 µg/L and control (96 h). Herbicide exposure lowered plasma bactericidal activity at both concentrations (24 h) and at 0.488 µg/L (96 h); and plasma complement activity declined at 4.88 µg/L comparing with 0.488 µg/L and control (96 h), and was lower at all concentrations at 96 h than at 24 h. Plasma K(+) levels were higher at 4.88µg/L than in the remaining groups (24 and 96h); and Na(+) levels decreased at 4.88 µg/L compared to control (96 h). Na(+)/K(+)-ATPase and H(+)-ATPase activities in gills were lower at 4.88 µg/L comparing with control (24 h) and with the respective concentration at 96 h; and AChE activity in brain was higher at 0.488 and 4.88 µg/L than control (24 h) and the respective concentrations at 96 h, while in muscle it was higher at 0.488 and 4.88 µg/L than control (96 h) and the respective concentrations at 24 h. The present findings demonstrate that, despite IMY+IMI targets the animal-absent AHAS enzyme, such formulation displayed an acute toxic effect upon R. quelen homeostasis by impacting on vital functions such as immune defense, metabolism, ionoregulation and neurotransmission.

Thiamethoxam induced hepatic energy changes in silver catfish via impairment of the phosphoryl transfer network pathway: Toxicological effects on energetics homeostasis.

Precise coupling of spatially separated intracellular adenosine triphosphate (ATP)-producing and ATP-consuming processes exerts a pivotal role in bioenergetic homeostasis of living organisms, and the phosphotransfer network pathway, catalyzed by adenylate kinase (AK) and pyruvate kinase (PK), is fundamental in cellular and tissue energetic homeostasis. Measurement of the phosphotransfer network can provide new information for understanding the alterations in hepatic energetic metabolism during exposition to insecticides, such as thiamethoxam. Therefore, the aim of this study was to evaluate whether exposition to thiamethoxam negatively affects the hepatic enzymes of the phosphotransfer network in silver catfish (Rhamdia quelen). Hepatic AK and PK activities were inhibited at 3.75 µg L-1 after 24 h of exposure and at 1.125 and 3.75 µg L-1 after 96 h of exposure compared with the control group. The hepatic ATP levels were decreased following 3.75 µg L-1 thiamethoxam treatment after 24 h of exposure and at 1.125 and 3.75 µg L-1 after 96 h of exposure compared with the control group. The enzymatic activity of the phosphotransfer network and ATP levels did not recover after 48 h of recovery in clean water. Thus, the inhibition of hepatic AK and PK activities by thiamethoxam caused impairment of energy homeostasis in liver tissue, decreasing hepatic ATP availability. Moreover, the absence of a mutual compensatory mechanism between these enzymes directly contributes to ATP depletion and to a severe energetic dysregulation, which may contribute to toxic effects caused by thiamethoxam.

Gill bioenergetics dysfunction and oxidative damage induced by thiamethoxam exposure as relevant toxicological mechanisms in freshwater silver catfish Rhamdia quelen.

Thiamethoxam is a neonicotinoid pesticide utilized on a worldwide scale, it has been reported in freshwater ecosystems, and detected in fishery products. Nevertheless, there is a lack of information about thiamethoxam sublethal effects on the gills of freshwater fish, principally linked to energetic metabolism. In this context, creatine kinase (CK) is an enzyme of the phosphoryl transfer network that provides a temporal and spatial energy buffer to maintain cellular energy homeostasis in tissues with high energy requirements, such as gills. Based on this evidence, the aim of this study was to evaluate whether exposure to thiamethoxam impairs the cytosolic and mitochondrial CK activities in gills of Rhamdia quelen, and the involvement of oxidative stress in the energetic imbalance. Branchial CK (cytosolic and mitochondrial) activity and sodium­potassium pump (Na+, K+-ATPase) were inhibited, and adenosine triphosphate (ATP) levels decreased after 96 h exposure to 1.125 and 3.75 µg/L thiamethoxam compared to the control group. Moreover, levels of branchial thiobarbituric acid reactive substances (TBARS) and protein carbonylation increased at 3.75 µg/L thiamethoxam after 96 h of exposure compared to the control group, while the non-protein thiol (NPSH) content did not differ between groups. It is important to emphasize that all evaluated parameters did not recover after 48 h in clean water. To summarize, the data presented here clearly demonstrated that thiamethoxan exposure severely impairs cytosolic and mitochondrial CK activities, a key enzyme for gill energy buffering to maintain cellular energy homeostasis, and this effect appears to be mediated by oxidation of lipid and protein molecules, which consequently thereby induces oxidative stress.