Exposure to cocaine and its main metabolites altered the protein profile of zebrafish embryos

Identifying sublethal endpoints for evaluating neurotoxic compounds utilizing the fish embryo toxicity test.

Applications of advanced neuro-behavioral analysis strategies in aquatic ecotoxicology.

Cadmium is a common heavy metal pollutant. Previous studies have found that long-term cadmium exposure can cause damage to multiple organs/systems in humans and experimental animals; however, there are few studies that elucidate its effects on offspring development, discuss whether it can be transmitted to offspring from the parent, and debate whether it affects the functional development of the thyroid hormone system in offsprings. In this study, sexually mature zebrafish were exposed to different concentrations of cadmium chloride (0.01 μmol/L, 0.1 μmol/L, and 1 μmol/L) to study reproductive toxicity. It was found that parental zebrafish exposed to 1 μmol/L of cadmium chloride produced offsprings with different degrees of malformation. At 5 days post-fertilization (dpf), the levels of 3,5,3′-triiododenosine (T3) and thyroxine (T4) in the zebrafish were decreased. At 10 dpf, the T4 and T3 levels in the zebrafish of the offspring were significantly reduced. At the same time, the expression of thyroid receptor (trα and trβ) genes in five dpf larvae was significantly up-regulated in the 1 μmol/L treatment group relative to the control group. The mRNAs of thyroid hormone synthesis and metabolism-related genes (tshβ, dio1, dio2, ugt1ab, and ttr) were significantly up-regulated in the 0.1 μmol/L and 1 μmol/L treatment groups. This study demonstrates that parental cadmium chloride exposure produces reproductive toxicity in zebrafish and that the effects can be transferred from the parent to the offspring, resulting in developmental toxicity in the thyroid endocrine system.

Parental exposure to cadmium chloride causes developmental toxicity and thyroid endocrine disruption in zebrafish offspring.

The longitudinal effects of early developmental cadmium exposure on conditioned place preference and cardiovascular physiology in zebrafish

A sizeable portion of the societal drain from cocaine abuse results from the complications of in utero drug exposure. Because of challenges in using humans and mammalian model organisms as test subjects, much debate remains about the impact of in utero cocaine exposure. Zebrafish offer a number of advantages as a model in longitudinal toxicology studies and are quite sensitive physiologically and behaviorally to cocaine. In this study, we have used zebrafish to model the effects of embryonic pre-exposure to cocaine on development and on subsequent cardiovascular physiology and cocaine-induced conditioned place preference (CPP) in longitudinal adults. Larval fish showed a progressive decrease in telencephalic size with increased doses of cocaine. These treated larvae also showed a dose dependent response in heart rate that persisted 24 h after drug cessation. Embryonic cocaine exposure had little effect on overall health of longitudinal adults, but subtle changes in cardiovascular physiology were seen including decreased sensitivity to isoproterenol and increased sensitivity to cocaine. These longitudinal adult fish also showed an embryonic dose-dependent change in CPP behavior, suggesting an increased sensitivity. These studies clearly show that pre-exposure during embryonic development affects subsequent cocaine sensitivity in longitudinal adults.

https://www.mdpi.com/1422-0067/17/6/847/pdf

Longitudinal Effects of Embryonic Exposure to Cocaine on Morphology, Cardiovascular Physiology, and Behavior in Zebrafish.

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The longitudinal effects of early developmental cadmium exposure on conditioned place preference and cardiovascular physiology in zebrafish

Longitudinal Effects of Embryonic Exposure to Cocaine on Morphology, Cardiovascular Physiology, and Behavior in Zebrafish.