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-  2018 

Tris-(2, 3-dibromopropyl) Isocyanurate Induced Oxidative Stress in the Human Neuronal Cell Lines and in Rat Brains
Tris-(2, 3-dibromopropyl) Isocyanurate Induced Oxidative Stress in the Human Neuronal Cell Lines and in Rat Brains

DOI: 10.15918/j.jbit1004-0579.17074

Keywords: tris-(2, 3-dibromopropyl) isocyanurate (TBC) oxidative stress human neuronal cell lines rat brain
tris-(2
, 3-dibromopropyl) isocyanurate (TBC) oxidative stress human neuronal cell lines rat brain

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Abstract:

Tris-(2, 3-dibromopropyl) isocyanurate (TBC) is a heterocyclic hexabrominated additive flame retardant, which is bio-accumulative, and can cause reproductive, endocrine disrupting, and neurotoxic effects. The present study was aimed at further evaluating the oxidative stress induced by TBC in the human neuronal cells and in rat brains. The results demonstrated that TBC caused apop-tosis of U251 and SH-SY5Y cells in a dose-and time-dependent manner and that U251 cells were more sensitive to TBC than that of SH-SY5Y cells. Meanwhile, 1 μg/mL of TBC can significantly in-duce the production of MDA in U251 cells, indicating that oxidative stress occurred after TBC short-term exposure (24 h). Similarly, in vivo administration of 0.5 mg/kg of TBC in rats for 7 days led to low growth rates and a significant increase of reactive oxygen species (ROS) and nitrogen species (RNS) in the brains. However, enzymes related to antioxidation, total superoxide dismutase (T-SOD) and reduced glutathione (GSH), were not affected obviously. This might indicate that 7-day exposure was not long enough to weaken antioxidant defence in the brains. Altogether, the results indicated that oxidative stress was induced by short-time TBC exposure.
Tris-(2, 3-dibromopropyl) isocyanurate (TBC) is a heterocyclic hexabrominated additive flame retardant, which is bio-accumulative, and can cause reproductive, endocrine disrupting, and neurotoxic effects. The present study was aimed at further evaluating the oxidative stress induced by TBC in the human neuronal cells and in rat brains. The results demonstrated that TBC caused apop-tosis of U251 and SH-SY5Y cells in a dose-and time-dependent manner and that U251 cells were more sensitive to TBC than that of SH-SY5Y cells. Meanwhile, 1 μg/mL of TBC can significantly in-duce the production of MDA in U251 cells, indicating that oxidative stress occurred after TBC short-term exposure (24 h). Similarly, in vivo administration of 0.5 mg/kg of TBC in rats for 7 days led to low growth rates and a significant increase of reactive oxygen species (ROS) and nitrogen species (RNS) in the brains. However, enzymes related to antioxidation, total superoxide dismutase (T-SOD) and reduced glutathione (GSH), were not affected obviously. This might indicate that 7-day exposure was not long enough to weaken antioxidant defence in the brains. Altogether, the results indicated that oxidative stress was induced by short-time TBC exposure.

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