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Published on: February 7, 2018
Antioxidants do not prevent acrylonitrile-induced toxicity
M P Carrera1, I Antolín, V Martín
1Instituto Universitario de Oncología del Principado de Asturias (IUOPA), Facultad de Medicina de la Universidad de Oviedo. c/Julian Clavería, 33006 Oviedo, Spain.
Toxicology Letters
|March 6, 2007
Summary
Acrylonitrile (ACN) toxicity involves oxidative stress, depleting glutathione (GSH). While N-acetylcysteine (NAC) protected cultured astrocytes, in vivo studies showed no brain oxidative damage in rats exposed to ACN.
Area of Science:
- Toxicology
- Neuroscience
- Biochemistry
Background:
- Acrylonitrile (ACN) toxicity is linked to oxidative stress mechanisms.
- ACN can deplete cellular glutathione (GSH) or be metabolized to cyanide.
- Understanding ACN's impact on cellular viability and oxidative damage is crucial.
Purpose of the Study:
- To investigate the effects of ACN on primary astrocyte viability and GSH levels.
- To evaluate the protective potential of various antioxidants against ACN-induced toxicity in vitro.
- To assess in vivo oxidative stress markers in the brains of rats exposed to ACN.
Main Methods:
- Primary astrocyte cultures were exposed to ACN (2.5mM) with or without antioxidants (taurine, NAC, trolox, estradiol, melatonin).
- Cell viability and GSH levels were measured in vitro.
- Wistar rats were exposed to ACN (200 ppm) for 14 days, followed by analysis of brain catalase activity, lipid peroxidation, and GSH concentration.
Main Results:
- In vitro, only N-acetylcysteine (NAC) effectively protected astrocytes from ACN-induced damage, highlighting GSH's role.
- Antioxidants like taurine, trolox, estradiol, and melatonin did not prevent ACN toxicity in astrocytes.
- In vivo, no significant oxidative damage was observed in the brains of ACN-exposed rats at the tested concentration.
Conclusions:
- Glutathione (GSH) plays a critical role in mitigating acrylonitrile (ACN) toxicity in primary astrocytes.
- N-acetylcysteine (NAC) demonstrates protective effects against ACN-induced astrocyte damage.
- Acrylonitrile exposure at 200 ppm for 14 days did not induce detectable oxidative stress in the rat brain.
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