Exposure to chlorpyrifos-cypermethrin combination during early development resulted in defective looping and ventricular noncompaction of heart in domestic chicken. The study was extended to elucidate the molecular basis of this novel observation. The primary culture of chicken embryonic heart cells showed a concentration-dependent loss of viability when challenged with this combination of technical-grade insecticides. Comet assay, DNA ladder assay, and analyses of appropriate markers at transcript and protein levels, revealed that chlorpyrifos-cypermethrin combination induced cell death by activating apoptosis. Parallelly, the tissues derived from control and experimental group hearts were checked for apoptotic markers, and the result was much similar to that of the in-vitro study. Further analysis showed that chlorpyrifos-cypermethrin combination deranged the expression pattern of the transcriptional regulators of cardiogenesis, namely TBX20, GATA5, HAND2, and MYOCD. This, together with heightened apoptosis, could well be the reason behind the observed structural anomalies in the heart of chlorpyrifos-cypermethrin poisoned embryos.

中文翻译：

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早期胚胎暴露于毒死蜱-氯氰菊酯组合诱导家鸡心脏模式缺陷

在早期发育过程中接触毒死蜱-氯氰菊酯组合导致家鸡心脏循环缺陷和心室致密化不全。该研究被扩展到阐明这一新观察的分子基础。鸡胚胎心脏细胞的原代培养物在受到这种技术级杀虫剂组合的挑战时表现出浓度依赖性的活力丧失。彗星试验、DNA 阶梯试验以及对转录物和蛋白质水平的适当标记物的分析表明，毒死蜱-氯氰菊酯组合通过激活细胞凋亡诱导细胞死亡。同时，对来自对照组和实验组心脏的组织进行凋亡标记检查，结果与体外研究的结果非常相似。进一步的分析表明，毒死蜱-氯氰菊酯组合扰乱了心脏发生转录调节因子的表达模式，即 TBX20、GATA5、HAND2 和 MYOCD。这与细胞凋亡增加一起很可能是在毒死蜱-氯氰菊酯中毒胚胎的心脏中观察到的结构异常背后的原因。