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

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 mu mol/L, 0.1 mu mol/L, and 1 mu mol/L) to study reproductive toxicity. It was found that parental zebrafish exposed to 1 mu mol/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 (tr alpha and tr beta) genes in five dpf larvae was significantly up-regulated in the 1 innol/L treatment group relative to the control group. The mRNAs of thyroid hormone synthesis and metabolism-related genes (tsh beta, dio1, dio2, ugt1ab, and ttr) were significantly up-regulated in the 0.1 mu mol/L and 1 mu mol/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.