Search

The extensive use of carbamate pesticides has led to a range of environmental and health problems, such as surface and groundwater contamination, and endocrine disorders in organisms. In this study, we focused on examining the effects of toxic exposure to the carbamate pesticide methomyl on the hatching, morphology, immunity and developmental gene expression levels in zebrafish embryos. Four concentrations of methomyl (0, 2, 20, and 200 μg/L) were administered to zebrafish embryos for a period of 96 h. The study found that exposure to methomyl accelerated the hatching process of zebrafish embryos, with the strongest effect recorded at the concentration of 2 μg/L. Methomyl exposure also trigged significantly reductions in heart rate and caused abnormalities in larvae morphology, and it also stimulated the synthesis and release of several inflammatory factors such as IL-1β, IL-6, TNF-α and INF-α, lowered the IgM contents, ultimately enhancing inflammatory response and interfering with immune function. All of these showed the significant effects on exposure time, concentration and their interaction (Time × Concentration). Furthermore, the body length of zebrafish exposed to methomyl for 96 h was significantly shorter, particularly at higher concentrations (200 μg/L). Methomyl also affected the expression levels of genes associated with development (down-regulated igf1, bmp2b, vasa, dazl and piwi genes), demonstrating strong developmental toxicity and disruption of the endocrine system, with the most observed at the concentration of 200 μg/L and 96 h exposure to methomyl. The results of this study provide valuable reference information on the potential damage of methomyl concentrations in the environment on fish embryo development, while also supplementing present research on the immunotoxicity of methomyl., Competing Interests: Declaration of Competing Interest The authors declare no conflicts of interest of this work., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Tilapia were exposed to 0, 0.2, 2, 20, 200 µg/L methomyl for 30 days, and then transferred to methomyl-free water for 18 days. Caspase-8 in serum, apoptosis rate, microstructure and ultra-microstructure of testis were checked after methomyl exposure and at 18 days after transferring to methomyl-free water. There were no significant changes in Caspase-8 activity, apoptosis rate, and tissue structure in testis exposed to 0.2 and 2 µg/L compared with control. However, when tilapia exposed to 20 and 200 µg/L, the Caspase-8 activity and apoptosis rate were induced significantly, and tissue damage happened compared with the control. Thus it would appear 2 µg/L methomyl might be considered as the no observed adverse effect level. Recovery data showed that the effects produced by lower concentration of 20 µg/L were reversible but not at the higher 200 µg/L concentration.

Tilapia were exposed to sub-lethal concentrations of 0, 0.2, 2, 20 or 200 μg/L for 30 days, then transferred to methomyl-free water for 18 days. E 2 , T, 11-KTand VTG in serum were examined. There were no significant changes in all the parameters in serum of tilapia exposed to 0.2 μg/L and 2 μg/L methomyl compared to the control. However, 20 μg/L and 200 μg/L have the potential to disrupt the endocrine system of male tilapia, as shown by its ability to increase VTG and E 2 and decrease T and 11-KT in serum. Thus it would appear the no observed adverse effect level for sexual steroid hormones of methomyl is lower than 2 μg/L. Recovery data showed that the effects produced by 20μg/L were reversible but not at 200μg/L. Furthermore, the sensitivity of above parameters to methomyl followed the order of VTG>E 2 >11-KT>T>GSI, suggesting VTG being the better biomarkers., (© 2017 Wiley Periodicals, Inc.)

Tilapia were exposed to sublethal methomyl concentrations of 0, 0.2, 2, 20 or 200 μg/L for 30 days, and then transferred to methomyl-free water for 18 days. The sexual steroid hormones 17β-estradiol (E2), testosterone (T), and 11-ketotestosterone (11-KT) in tilapia testes were examined at 0, 6, 12, 18, 24 and 30 days after methomyl exposure, and at 18 days after fish were transferred to methomyl-free water. There were no significant changes in the hormone parameters in testes of tilapia exposed to low concentration 0.2 and 2 μg/L methomyl compared with the controls. However, high concentration 20 and 200 μg/L methomyl had the potential to disrupt the endocrine system of male tilapia, as shown by an increase in E 2 and a decrease in T and 11-KT in the testes. Thus, it would appear that the 2 μg/L methomyl might be considered the no-observed-adverse-effect level. Recovery data showed that the effects produced by the lower concentration of 20 μg/L were reversible but the effects were not reversible at the higher concentration of 200 μg/L.

The present study clearly showed that chronic exposure to polychlorinated biphenyls (PCBs) at environmentally relevant concentrations can damage juvenile tilapia livers by modulating antioxidant enzyme activities and gene transcription, which affects toxic bioaccumulation and histological congestion. The results suggest that PCBs caused a decrease in the activity of some hepatic antioxidative and biotransformation enzymes (SOD, CAT, GST, T-GSH, and MDA) in tilapia at 7 days, as well as transcriptional changes (sod, cat, and gst). Except for some antioxidant parameters (T-GSH, GSH/GSSG, T-AOC, and MDA), significant declines and increases occurred at 14 and 21 days, respectively. Most of the antioxidant enzymatic signatures and genotoxicity significantly increased at 14 and 21 days. This study presented evidence that PCBs could result in hepatic toxicity through oxidative stress in the early growth stages of tilapia, and we speculated that oxidative stress plays an important role in embryonic developmental toxicity induced by PCBs., Competing Interests: The authors declare no conflict of interest.

Hepatic antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) of Nile tilapia in response to pesticide methomyl and recovery pattern were researched by exposing tilapia to sub-lethal methomyl concentrations of 0, 0.2, 2, 20 and 200 μg/L for 30 days, and then transferred to methomyl-free water for 18 days. Hepatic SOD and CAT were measured at 10 min (day 0), 6, 12, 18, 24 and 30 days after starting the experiment and at 18 days after transferring to methomyl-free water. The results showed hepatic SOD and CAT activities in 2, 20 and 200 μg/L groups were affected significantly, however, that in 0.2 μg/L group didn't change significantly compared to control during 30-day exposure period. Thus it would appear the 0.2 μg/L methomyl might be considered the no observed adverse effect level. Recovery data showed that, for SOD, the effects produced by lower concentration of methomyl 2 μg/L were reversible but not at concentrations higher than 20 μg/L, however, for CAT, the effects produced by all the concentrations were reversible.

The chronic effect of methomyl on the antioxidant system in tilapia (Oreochromis niloticus) was investigated. Fish were exposed to sub-lethal concentrations of 0.2, 2, 20 and 200μgL(-1) for 30 days, and then transferred to methomyl-free water for 18 days. Hepatic antioxidant parameters, including Glutathione-S-transferase (GST), Glutathione peroxidase (GPx), Glutathione reductase (GR), Reduced glutathione (GSH) and oxidized glutathione (GSSG), were measured at 10min (day 0), 6, 12, 18, 24 and 30 days after starting the experiment and at 18 days after transferring to methomyl-free water. There were no significant changes in enzymatic activity and content of antioxidants in liver of tilapia exposed to 0.2μgL(-1) methomyl compared to controls. However, the results showed significant increases in activities of GST, GR, GPx and levels of GSSG accompanied by a decrease in GSH levels following methomyl exposure in tilapia to 2, 20 or 200μgL(-1) over the 30-day exposure period and the highest induction rates in GST, GR, GPx and GSSG were 150.87%, 163.21%, 189.76%, and 179.56% of the control respectively, and the highest inhibition rate in GSH was 50.67% of the control, suggesting the presence of oxidative stress. Thus it would appear that the 0.2μgL(-1) methomyl might be considered as the no observed adverse effect level (NOAEL). Recovery data showed that the effects produced by lower concentration of methomyl 20μgL(-1) were reversible but not at the higher 200μgL(-1) concentration., (© 2013 Published by Elsevier Inc.)

Tilapia were exposed to sublethal methomyl concentrations of 0, 0.2, 2, 20, or 200 μg/L for 30 d, and then were transferred to methomyl-free water for 18 d. Renal antioxidant parameters, including catalase (CAT), superoxide dismutase (SOD), glutathione S-transferase (GST), glutathione peroxidase (GPx) , glutathione reductase (GR), total glutathione (GSH), and reduced glutathione (GSSG), were examined in tilapia at d 0, 6, 12, 18, 24, and 30 after starting the experiment and at 18 d after transferring to methomyl-free water. There were no significant changes in enzymatic activity and content of antioxidants in kidney of tilapia exposed to 0.2 μg/L methomyl compared to controls. The results showed significant increases in SOD, CAT, GST, GR, GPx, and level of GSSG accompanied by a decrease in GSH levels following methomyl exposure in tilapia to 2, 20, or 200 μg/L over the 30-d exposure period, suggesting the presence of oxidative stress. Thus, it would appear the 0.2 μg/L methomyl might be considered the no-observed-adverse-effect level (NOAEL). Recovery data showed that the effects produced by lower concentration of methomyl at 20 μg/L were reversible but not at the higher 200 μg/L concentration.