Nanotechnology-based pesticides: Environmental fate and ecotoxicity.

The imminent increase in global food demand inevitably leads to an increase in agricultural practices, with an emphasis on pesticide applications. Nanotechnology-based pesticides, or nanopesticides, have gained importance as they are more efficient and, in some cases, less toxic than their conventional counterparts. However, concerns about these novel products have arisen as evidence about their (eco)safety is controversial. This review aims to: (1) introduce the currently applied nanotechnology-based pesticides and their mechanisms of toxic action; (2) describe their fate when released into the environment, with an emphasis on aquatic environments; (3) summarize available research on ecotoxicological studies in freshwater non-target organisms through a bibliometric analysis; and (4) identify gaps in knowledge from an ecotoxicological perspective. Our results show that the environmental fate of nanopesticides is poorly studied and depends on both intrinsic and external factors. There is also a need for comparative research into their ecotoxicity between conventional pesticide formulations and their nano-based counterparts. Among the few available studies, most considered fish species as test organisms, compared to algae and invertebrates. Overall, these new materials generate toxic effects on non-target organisms and threaten the integrity of the environment. Therefore, deepening the understanding of their ecotoxicity is crucial.

Low temperature stress in a cultured fish (Piaractus mesopotamicus) fed with Pyropia columbina red seaweed-supplemented diet.

This study aimed to analyze the cold stress effects (in terms of hematology, energy reserves, and oxidative stress) in Piaractus mesopotamicus (pacú) and their mitigation by a Pyropia columbina red seaweed-supplemented diet. For this purpose, juvenile fish were fed with a control (CD) or a red seaweed-supplemented diet (RD) for 60 days, and then, the animals were exposed to a low temperature (14 °C) and a control temperature (24 °C) for 24 h. The cold shock generated an increase of hemoglobin levels in fish fed with both diets. In CD-fed fish, plasmatic triglycerides, cholesterol, and hepatic glycogen decreased after the thermal shock; meanwhile, the animals fed with RD showed decreased hepatic proteins, but increased cholesterol and hepatic glycogen. Regarding oxidative stress, antioxidant enzymes augmented their activity in the liver, intestine, and gills; meanwhile, lipid oxidative damage was observed in the liver and intestine of fish exposed to 14 °C and fed with both diets. Pacú was sensitive to cold shock, but no mitigation effects were observed in fish fed with the supplemented diet. Further research should target higher concentrations of P. columbina in supplemented diets to take advantage of this valuable resource.

Effects of cold stress on juvenile Piaractus mesopotamicus and the mitigation by ß-carotene.

This study investigated the effects of cold stress on morphometrical and hematological biomarkers, energy metabolism, and oxidative stress in different tissues of P. mesopotamicus, and the protective role of ß-carotene. Fish were fed with a control diet (CD) and the same diet supplemented with 105 mg/kg ß-carotene (BD) for 60 days. After the feeding trial, fish fed CD or BD diets were exposed to control (24 °C) and low temperature (14 °C) for 24 h. Fish (CD and BD) exposed to thermal stress showed lower hepatosomatic index. The hemoglobin increased only in CD-fed fish exposed to 14 °C. Increased glycemia, plasmatic protein depletion, and decreased hepatic glycogen were observed in fish fed the CD, while only the lipid levels in liver were augmented in BD-fed fish exposed at 14 °C. Regarding the oxidative stress, increased antioxidant enzymes activity and lipid peroxidation were observed in CD-fed fish exposed to cold. The two-way ANOVA showed an interaction between dietary treatment and temperature for glucose and oxidative stress biomarkers, with the highest values recorded in 14 °C-exposed fish fed with the CD. Our study demonstrated that cold stress had the greatest impact on fish oxidative status, and ß-carotene reduces harmful effects induced by cold in P. mesopotamicus.

Dietary chia seed induced changes in hepatic transcription factors and their target lipogenic and oxidative enzyme activities in dyslipidaemic insulin-resistant rats.

The present study analyses the effect of dietary chia seed rich in n-3 α-linolenic acid on the mechanisms underlying dyslipidaemia and liver steatosis developed in rats fed a sucrose-rich diet (SRD) for either 3 weeks or 5 months. The key hepatic enzyme activities such as fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), glucose-6-phosphate dehydrogenase (G-6-PDH), carnitine palmitoyltransferase-1 (CPT-1) and fatty acid oxidase (FAO) involved in lipid metabolism and the protein mass levels of sterol regulatory element-binding protein-1 (SREBP-1) and PPARα were studied. (1) For 3 weeks, Wistar rats were fed either a SRD with 11 % of maize oil (MO) as dietary fat or a SRD in which chia seed replaced MO (SRD+Chia). (2) A second group of rats were fed a SRD for 3 months. Afterwards, half the rats continued with the SRD while for the other half, MO was replaced by chia for 2 months (SRD+Chia). In a control group, maize starch replaced sucrose. Liver TAG and the aforementioned parameters were analysed in all groups. The replacement of MO by chia in the SRD prevented (3 weeks) or improved/normalised (5 months) increases in dyslipidaemia, liver TAG, FAS, ACC and G-6-PDH activities, and increased FAO and CPT-1 activities. Protein levels of PPARα increased, and the increased mature form of SREBP-1 protein levels in the SRD was normalised by chia in both protocols (1 and 2). The present study provides new data regarding some key mechanisms related to the fate of hepatic fatty acid metabolism that seem to be involved in the effect of dietary chia seed in preventing and normalising/improving dyslipidaemia and liver steatosis in an insulin-resistant rat model.

Ecotoxicity of silica nanoparticles in aquatic organisms: An updated review.

This review aims to (i) provide a current overview of the main characteristics of SiNP (physical and chemical properties, applications, and emissions), (ii) evaluate the scientific production up to date concerning SiNP, with focus on their toxic effects, through a bibliometric analysis, (iii) describe the main toxic mechanisms of SiNP, (iv) assess the current knowledge about ecotoxicity of SiNP on aquatic organisms (marine and freshwater), and (v) identify the main gaps in the knowledge of SiNP toxicity from an environmentally point of view. The scientific production of SiNP concerning their chemical and physical characteristics has increased exponentially. However, little information is available regarding their ecotoxicity. Particle functionalization is a key factor that reduces SiNP toxicity. Most of the studies employed standard species as test organisms, being the local/native ones poorly represented. Further studies employing long-term exposures and environmentally relevant concentrations are needed to deepen the knowledge about this emergent pollutant.

Lipogenic enzyme activities and glucose uptake in fat tissue of dyslipemic, insulin-resistant rats: effects of fish oil.

OBJECTIVE: The purposes of the present work were twofold: (1) investigate same mechanisms involved in the development of fat cell hypertrophy in the experimental model of dyslipidemia and whole-body insulin resistance induced in rats chronically fed a sucrose-rich diet (SRD); and (2) analyze the possible beneficial effect of fish oil on these mechanisms. METHODS: For 6 mo, male Wistar rats received a sucrose-rich diet (62.5% w/w sucrose, 8% corn oil) or a control diet in which sucrose was replaced by starch. After this period, the sucrose-fed animals were divided randomly into two groups: the first one continued with the same diet up to 8 mo and the second one received the same diet, but with corn oil replaced by 7% fish oil+1 % corn oil. Rats were fed with this diet for the next 2 mo. RESULTS: Although an enlarged fat cell lipolysis and an impaired insulin-stimulated glucose uptake were present in the fat cells of SRD-fed rats, an increase of several key enzymes of the novo lipogenesis could be one of the possible mechanisms involved in visceral adiposity. The addition of dietary fish oil restored or improved the above abnormalities. CONCLUSION: This study shows possible mechanisms conditioning the influence of nutrients on the development and management of dyslipidemia, insulin sensitivity, and fat cell accretion, all abnormalities present in the metabolic syndrome.

Dietary fish oil positively regulates plasma leptin and adiponectin levels in sucrose-fed, insulin-resistant rats.

Insulin resistance and adiposity induced by a long-term sucrose-rich diet (SRD) in rats could be reversed by fish oil (FO). Regulation of plasma leptin and adiponectin levels, as well as their gene expression, by FO might be implicated in these findings. This study was designed to evaluate the long-term regulation of leptin and adiponectin by dietary FO in a dietary model of insulin resistance induced by long-term SRD in rats and to determine their impact on adiposity and insulin sensitivity. Rats were randomized to consume a control diet (CD; n = 25) or an SRD (n = 50) for 7 mo. Subsequently, the SRD-fed rats were randomized to consume SRD+FO or to continue on SRD for an additional 2 mo. Long-term SRD induced overweight and decreased both plasma leptin and adiponectin levels without change in gene expression. Dyslipidemia, adiposity, and insulin resistance accompanied these modifications. Shifting the source of fat to FO for 2 mo increased plasma levels of both adipokines, reversed insulin resistance and dyslipidemia, and improved adiposity. These results were not associated with modifications in gene expression. These results suggest that increasing both adipokines by dietary FO might play an essential role in the normalization of insulin resistance and adiposity in dietary-induced, insulin-resistant models.