Assessment of the acute acrylonitrile-induced neurotoxicity in rats
References (23)
- et al.
Studies on the mechanism of acrylonitrile neurotoxicity
Toxicol. Appl. Pharmacol.
(1979) - et al.
Acrylonitrile in vivo metabolism in rats and mice
Drug Metab. Dispos.
(1981) - et al.
Influence of sulfhydryls reagents and heavy metals on the functional state of the muscarinic acetylcholine receptors in rat brain
Mol. Pharmacol.
(1977) - et al.
Primary brain tumors in Fischer 344 rats chronically exposed to acrylonitrile in drinking water
Food Chem. Toxicol.
(1986) - et al.
Toxicity of acrylonitrile (vinyl cyanide) I. A study of the acute toxicity
J. Ind. Hyg. Toxicol.
(1942) - et al.
Regulation of muscarinic receptor binding of guanine nucleotides and N-ethylmaleimide
J. Supramol. Struct.
(1980) - et al.
Effect of acute acrylonitrile exposure on metrazol induced seizures in the rat
Neurotoxicology
(1985) - et al.
Molecular interactions of acrylonitrile and potassium cyanide with rat blood
Chem. Biol. Interact.
(1982) - et al.
Hemoglobin degradation, lipid peroxidation and inhibition of Na+/K+-ATPase in rat erythrocytes exposed to acrylonitrile
J. Biochem. Toxicol.
(1990) - et al.
Metabolism of acrylonitrile by isolated rat hepatocytes
Cancer Res.
(1984)
In vivo biotransformation and biliary excretion of 1-14C acrylonitrile in rats
Arch. Toxicol.
Cited by (27)
Multibiomarker interactions to diagnose and follow-up chronic exposure of a marine crustacean to Hazardous and Noxious Substances (HNS)
2018, Environmental PollutionCitation Excerpt :Two antagonistic sets of motoneurons innervate, in fact, the scaphognathite depressor and levator muscles controlling the ventilatory appendages (Simmers and Bush, 1983). ACN is a known Central Nervous System (CNS) depressant (Rocha et al., 2016), which in mammals can cause cholinergic toxicity through acetylcholine (ACh) mimetics and AChE inhibition (Ghanayem et al., 1991). Furthermore, in mice, ACN may compromise cell's capacity to deal with the stress, leading to a decrease in AChE activity (Yuanqing et al., 2013).
Differential protection of pre- versus post-treatment with curcumin, Trolox, and N-acetylcysteine against acrylonitrile-induced cytotoxicity in primary rat astrocytes
2015, NeuroToxicologyCitation Excerpt :Acrylonitrile (AN) is an extensively manufactured aliphatic nitrile used in the synthesis of acrylic fiber, resins and plastics and in the manufacture of soft prosthesis material, highly permeable dialysis tubing and medical gloves (IARC, 1999). Although the nervous system response to acute AN exposure exhibits characteristics analogous to acute cyanide poisoning, the exact mechanism(s) of AN-induced neurotoxicity has yet to be fully defined (Enongene et al., 2000; Ghanayem et al., 1991). Oxidative stress may be involved in AN-induced neurotoxicity secondary to depletion of antioxidants and/or increased production of reactive oxygen species (ROS).
Simulation of a hazardous and noxious substances (HNS) spill in the marine environment: Lethal and sublethal effects of acrylonitrile to the european seabass
2013, ChemosphereCitation Excerpt :Fish from the 2 mg L−1 acrylonitrile exposure presented the skin extremely dark and impairment of swimming performance, characterized by low swimming activity with uncontrolled circular movements at the top of the aquarium, together with bumps with the aquarium walls. The swimming performance observed in fish at the highest acrylonitrile exposure dose, suggest an impact in the nervous system, which integrates well with the observations in mammals (Ghanayem et al., 1991; Gagnaire et al., 1998; Esmat et al., 2007). However, understanding the mechanisms underlying a potential effect on fish nervous system requires further investigation through the measurement of neurotoxic parameters such as cholinesterase activity in fish brain.
Elevation of 4-hydroxynonenal and malondialdehyde modified protein levels in cerebral cortex with cognitive dysfunction in rats exposed to 1-bromopropane
2013, ToxicologyCitation Excerpt :In principle and where possible, the administration route in animal experiments should be relevant to anticipated human exposure. As one of the most convenient and accurate route of administration (Andersen, 2003; Perera et al., 1989), gavage had also been employed in the studies of 1-BP (Lee et al., 2005, 2010) and other volatile neurotoxicants such as ethylbenzene (Mellert et al., 2007), acrylonitrile (Ghanayem et al., 1991), styrene (Chakrabarti, 2000) and BDE-99 (Bellés et al., 2010). However the rats exposed to 1-BP by gavage exhibited similar neurotoxic symptoms observed in human cases.
- 1
Present address: NIH/NIEHS, RTP, NC.
- 2
Present address: Department of Biology, University of Texas Pan American, Edinburg, TX.
- 3
Present address: Cairo, Egypt.
- 4
Present address: U.S. EPA, Cincinnati, OH.