EurekaMag.com logo
+ Site Statistics
References:
53,869,633
Abstracts:
29,686,251
+ Search Articles
+ Subscribe to Site Feeds
EurekaMag Most Shared ContentMost Shared
EurekaMag PDF Full Text ContentPDF Full Text
+ PDF Full Text
Request PDF Full TextRequest PDF Full Text
+ Follow Us
Follow on FacebookFollow on Facebook
Follow on TwitterFollow on Twitter
Follow on LinkedInFollow on LinkedIn

+ Translate

Free radicals and ethanol-induced cytotoxicity in neural crest cells



Free radicals and ethanol-induced cytotoxicity in neural crest cells



Alcoholism Clinical & Experimental Research. 20(6): 1071-1076



Associations between ethanol-induced cranial neural crest cell (NCC) damage in mammalian embryos and subsequent malformations as observed in human fetal alcohol syndrome have previously been illustrated. The vulnerability of NCCs to this teratogen may result, at least in part, from their sensitivity to free radical damage. To examine relationships between free radical generation and NCC cytotoxicity, primary culture of mouse NCCs was used. NCC viability was determined in both dose- and time-response studies involving ethanol exposure. After 48 hr of culture, cell viability was significantly diminished at all doses tested (i.e., 50, 100, 150, and 200 mM ethanol). At 100 mM ethanol (a dosage that is teratogenic in vivo and in whole embryo culture), cell viability decreased to apprx 50% of control values over the first 12 hr of culture, and decreased further, to apprx 20% by 48 hr. Using nitroblue tetrazolium as a probe, it was observed that exposure of NCCs to ethanol stimulated the production of superoxide anion radicals. Co-treatment of the ethanol-exposed NCCs with free radical scavengers including 300 units/ml of superoxide dismutase, catalase (500 units/ml), or alpha-tocopherol (300 mu-M) significantly improved NCC viability. These results suggest that the ethanol-induced NCC injury is mediated, at least in part, through the generation of free radicals. To test this hypothesis further, NCCs were exposed in culture to xanthine/xanthine oxidase. Exogenous free radicals generated by the xanthine/xanthine oxidase system resulted in reduced NCC viability, the severity of which increased in a time and enzyme concentration-related manner. Superoxide dismutase (300 units/ml) and catalase (500 units/ml) significantly reduced the effects of the xanthine/xanthine oxidase-generated free radicals on NCC viability. The similarity between the susceptibility of NCCs to ethanol and their susceptibility to exogenous free radicals in concert with the free radical scavenger-mediated amelioration of ethanol and exogenous free radical-induced NCC death strongly suggest that free radicals play a significant role in ethanol-induced NCC death.

(PDF emailed within 0-6 h: $19.90)

Accession: 008703620

Download citation: RISBibTeXText

PMID: 8892529

DOI: 10.1111/j.1530-0277.1996.tb01948.x



Related references

The role of free radicals in ethanol-induced neural crest cell death. Teratology 51(3): 181, 1995

Ethanol induces the generation of reactive free radicals by neural crest cells in vitro. Journal of Craniofacial Genetics and Developmental Biology 10(3): 277-293, 1990

Free radicals superoxide dismutase and neural crest cells. Journal of Dental Research 68(SPEC ISSUE): 295, 1989

Effects of ethanol on cranial neural crest cells Evidence of selective elimination by ethanol-induced apoptosis. FASEB Journal 8(4-5): A953, 1994

Iron mediated free radical generation and ethanol-induced neural crest cell toxicity. Alcoholism Clinical & Experimental Research 23(5 SUPPL ): 65A, 1999

Iron-mediated free radical injury in ethanol-exposed mouse neural crest cells. Journal of Pharmacology and Experimental Therapeutics 294(1): 134-140, 2000

Irreversible morphological and dynamic changes induced by ethanol in neural crest cells. Alcoholism Clinical & Experimental Research 23(5 SUPPL ): 29A, 1999

Changes of morphological parameters of in vitro migrating neural crest cells induced by ethanol. Comunicaciones Biologicas 14(2): 141-149, 1996

Differential sensitivity of mouse neural crest cells to ethanol-induced toxicity. Alcohol 20(1): 75-81, 2000

Involvement of seven in absentia homolog-1 in ethanol-induced apoptosis in neural crest cells. Neurotoxicology and Teratology 46: 26-31, 2015

Relationship of early changes in oxygen free radicals and intracellular free calcium to cytotoxicity in cerebellar granule cells induced by metals. Journal of Neurochemistry 69(SUPPL ): S157, 1997

Role of early migratory neural crest cells in developmental anomalies induced by ethanol. International Journal of Developmental Biology 39(2): 421-422, 1995

Laser scanning confocal microscopic visualization of free radical generation and cell death in ethanol-exposed living neural crest cells. Teratology 55(1): 62, 1997

MiR-125b protects against ethanol-induced apoptosis in neural crest cells and mouse embryos by targeting Bak 1 and PUMA. Experimental Neurology 271: 104-111, 2015

Ethanol-induced morphological and dynamic changes of neural crest cells Further contribution to the etiopathogeny of fetal alcohol syndrome. Molecular Biology of the Cell 7(SUPPL ): 486A, 1996