4.5 Article

Di-2-ethylhexyl phthalate-induced neurobehavioural transformation is associated with altered glutathione biosynthesis and neurodegeneration in zebrafish brain

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FISH PHYSIOLOGY AND BIOCHEMISTRY
卷 49, 期 3, 页码 501-514

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SPRINGER
DOI: 10.1007/s10695-023-01197-2

关键词

DEHP; Neurobehavioural response; Oxidative stress; Chromatin condensation

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The contamination of life-sustaining environments with synthetic pollutants, such as di-2-ethylhexyl phthalate (DEHP), has increased at an alarming rate. DEHP, commonly found in plastics, can cause reproductive toxicity, disrupt the thyroid endocrine system, and induce oxidative stress and neurodevelopmental defects. This study focused on the neurobehavioral effects of DEHP on zebrafish and found that it acts as a neurotoxicant by inducing oxidative stress and altering the glutathione biosynthetic pathway. Chronic exposure to DEHP also resulted in neuronal pyknosis and chromatin condensation in the zebrafish brain. Overall, the study suggests the potential role of DEHP in inducing neuropathological manifestations and highlights the need for further research on the neuroprotective efficacy of natural compounds.
The contamination of life-sustaining environments with synthetic pollutants such as plastic-derived compounds has increased at an alarming rate in recent decades. Among such contaminants, di-2-ethylhexyl phthalate (DEHP) is an extensively used compound in plastics and plastic products to make them flexible. DEHP causes several adverse effects such as reproductive toxicity leading to infertility, miscarriage and litter size reduction, disruption of the thyroid endocrine system, oxidative stress, neurodevelopmental defect and cognitive impairment. An aquatic environment is a fragile site, where the accumulation of DEHP poses a significant threat to living organisms. In this context, the present study focused on whether the neurobehavioural transformation following exposure to DEHP is an outcome of augmented oxidative stress and neuromorphological alteration in the zebrafish brain. Our preliminary findings advocate that DEHP acts as a typical neurotoxicant in inducing neurobehavioural transformation in zebrafish. Furthermore, our study also supports the idea that DEHP itself acts as a potent neurotoxicant by altering the glutathione biosynthetic pathway through the induction of oxidative stress in the zebrafish brain. Similarly, our findings also link the abovementioned neurobehavioural transformation and oxidative stress with augmented neuronal pyknosis and chromatin condensation in the periventricular grey zone of the zebrafish brain following chronic exposure to DEHP. Therefore, the overall conclusion of the present study advocates the potential role of DEHP in inducing neuropathological manifestation in the zebrafish brain. Future research directed towards elucidating the neuroprotective efficacy of natural compounds against DEHP-induced neurotoxicity may provide a new line of intervention.

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