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Chemosphere ; 253: 126762, 2020 Aug.
Article in English | MEDLINE | ID: mdl-32302915

ABSTRACT

17ß-trenbolone (17ß-TBOH) is one of the dominant metabolites of trenbolone acetate, which is widely applied in beef cattle operations around the globe. The effects of environmental concentrations of 17ß-trenbolone on the early development of zebrafish embryos have received very little attention. Melatonin could regulate sleep-wake cycle and plays a protective role in various adverse conditions. Here, environmentally realistic concentrations of 17ß-trenbolone (1 ng/L, 10 ng/L, 50 ng/L) has been exposure to zebrafish embryos at 2 h postfertilization (hpf). The results showed that 10 ng/L and 50 ng/L 17ß-trenbolone disturbed the distribution of caudal primary motoneurons and downregulated expression of motoneuron development related genes along with locomotion decreasing. While melatonin could recover the detrimental effects caused by 17ß-trenbolone. Interestingly, 17ß-trenbolone exposure increased waking activity and decreased rest even in a low dose (1 ng/L). Moreover, it upregulated hypocretin/orexin (Hcrt) signaling which promotes wakefulness. Melatonin restored the insomnia-like alternation induced by 17ß-trenbolone exposure. Collectively, we conclude that 17ß-trenbolone disturbed motoneuron development and altered sleep/wake behavior, while melatonin could alleviate the deleterious influence on motoneuron development and recover the circadian rhythm.


Subject(s)
Behavior, Animal/drug effects , Environmental Pollutants/toxicity , Melatonin/pharmacology , Motor Activity/drug effects , Sleep Initiation and Maintenance Disorders/prevention & control , Trenbolone Acetate/toxicity , Zebrafish , Animals , Cattle , Circadian Rhythm/drug effects , Circadian Rhythm/genetics , Embryo, Nonmammalian/drug effects , Embryo, Nonmammalian/physiology , Embryonic Development/drug effects , Gene Expression Regulation, Developmental/drug effects , Motor Neurons/drug effects , Orexins/genetics , Phenotype , Sleep Initiation and Maintenance Disorders/chemically induced
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