Carbendazim exposure induces developmental, biochemical and behavioural disturbance in zebrafish embryos

Abstract

Carbendazim is a widely used broad spectrum benzimidazole fungicide; however, its effects to non-target aquatic organisms are poorly studied. The aim of this study was to investigate the toxic effects of carbendazim to zebrafish early life stages at several levels of biological organization, including developmental, biochemical and behavioural levels. The embryo assay was done following the OECD guideline 236 and using a concentration range between 1.1 and 1.8mg/L. Lethal and developmental endpoints such as hatching, edemas, malformations, heart beat rate, body growth and delays were assessed in a 96h exposure. A sub-teratogenic range (from 0.16 to 500μg/L) was then used to assess effects at biochemical and behavioural levels. Biochemical markers included cholinesterase (ChE), glutathione-S-transferase (GST), lactate dehydrogenase (LDH) and catalase (CAT) and were assessed at 96h. The locomotor behaviour was assessed using an automated video tracking system at 120h. Carbendazim (96h-LC50 of 1.75mg/L) elicited several developmental anomalies in zebrafish embryos with EC50 values ranging from 0.85 to 1.6mg/L. ChE, GST and LDH activities were increased at concentrations equal or above 4μg/L. The locomotor assay showed to be extremely sensitive, detecting effects in time that larvae spent swimming at concentrations of 0.16μg/L and thus, being several orders of magnitude more sensitive that developmental parameters or lethality. These are ecological relevant concentrations and highlight the potential of behavioural endpoints as early warning signs for environmental stress. Further studies should focus on understanding how the behavioural disturbances measured in these types of studies translate into fitness impairment at the adult stage.

Electrochemical remediation of amoxicillin: detoxification and reduction of antimicrobial activity

“…A similar fact occurred with LDH, a key enzyme in the anaerobic pathway of energy production. LDH acts as a cell injury marker at tissues, particularly when high levels of energy are required in a short period of time as in case of chemical stress conditions [42,[44][45][46]. In the present work, AMX significantly inhibited LDH, which may indicate a decreased glycolytic capacity in zebrafish larvae or suggest cellular necrosis leading to enzyme leakage and/or enzyme inhibition [45].…”

“…Considering that GST is an enzyme that plays an important role in phase II of the detoxification process, responsible for the biotransformation of xenobiotic compounds and acts a marker of antioxidant mechanisms [42][43][44][45], our results showed that AMX inhibited the detoxification process and the antioxidant activity in the embryonic stage of zebrafish. A similar fact occurred with LDH, a key enzyme in the anaerobic pathway of energy production.…”

Embryonic development, locomotor behavior, biochemical, and epigenetic effects of the pharmaceutical drugs paracetamol and ciprofloxacin in larvae and embryos of Danio rerio when exposed to environmental realistic levels of both drugs

“…The total distance was the statistically analyzed parameter and it consisted of the total swimming distance of the larvae during each measurement period. The methodology followed here was based on a previously described protocol …”

Multigenerational effects of carbendazim in Daphnia magna: From a subcellular to a population level

“…Increases in ChE activity in D. magna exposed to low concentrations of cadmium and the carbamate propoxur have been reported (Printes and Callaghan ; Jemec et al ), which could have been related to compensatory mechanisms following the disruption of homeostasis (Calabrese and Baldwin ). Andrade et al () observed an increase in ChE activity after exposure of zebrafish ( Danio rerio ) embryos to carbendazim, which the authors hypothesized to be related to apoptosis mechanisms; Jiang et al () found that this increase was associated with the induction of gene expression related to apoptosis. Even though the exact mechanisms are not yet understood, Jiang and Zhang () have theorized that ChE participates in the regulation of apoptosis and cell proliferation.…”