The cytotoxicity of short-chain alcohols and aldehydes in cultured neuroblastoma cells

Koerker, Robert L.; Berlin, Alan J.; Schneider, F. Howard

doi:10.1016/0041-008x(76)90091-0

Cited by 29 publications

(5 citation statements)

References 9 publications

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“…Scott et al (1986) reported that the in vitro survival of postmitotic mouse sensory neurons was decreased by ethanol exposure at concentrations of more than 1000 mg/dl. A study with mouse neuroblastoma reported that a very high concentration of ethanol (more than 2 M, 9200 mg/dl) was required to reduce cell viability by 50% (Koerker et al, 1976). In contrast, other in vitro studies have not observed ethanol-induced death of neurons.…”

Section: Ethanol-induced Cell Deathmentioning

confidence: 97%

Ethanol Induces Cell Death and Cell Cycle Delay in Cultures of Pheochromocytoma PC12 Cells

Luo

West

Cook

et al. 1999

Alcoholism Clin & Exp Res

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Animal models have clearly established that ethanol exposure can deplete neurons in the developing nervous system. However, the mechanism by which ethanol reduces cell number is unclear. In our study, cultures of pheochromocytoma cells, a neuronal-like cell line, were maintained in media, which supported cell proliferation. Although cell numbers continued to increase in the presence of ethanol, this increase was partially inhibited by ethanol exposure. This inhibitory effect was concentration and duration dependent. Cell proliferation was still partially inhibited after removal of ethanol, but this inhibition was temporary and disappeared after a 24-hr recovery period in ethanol-free conditions. Further study indicated that ethanol partially inhibited the increase in cell numbers by two mechanisms: (1) studies with vital stains indicated that ethanol induced cell death; (2) experiments using synchronized pheochromocytoma cell cultures showed that ethanol can induce cell cycle delay, thereby lengthening the doubling time of the cells. Analysis by flow cytometry indicated that with ethanol exposure, the cells accumulated in the G1 phase of the cell cycle. Our results suggest that in the developing nervous system, ethanol may limit the numbers of proliferating, neuronal precursor cells by two simultaneous mechanisms, cell death and cell cycle delay.

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Section: Ethanol-induced Cell Deathmentioning

confidence: 97%

Ethanol Induces Cell Death and Cell Cycle Delay in Cultures of Pheochromocytoma PC12 Cells

Luo

West

Cook

et al. 1999

Alcoholism Clin & Exp Res

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“…Of the four compounds that we tested, the following two do not induce peripheral neuropathy: ( 1) propionamide, which lacks the conjugated double bond acrylyl moiety often associated with toxicity (Koerker et al, 1976), and (2) methylene-bis-acrylamide, which has two acrylyl moieties and is systemically more toxic than acrylamide (Edwards, 1975a;Schotman et al, 1978). As expected, propionamide was inert in all our tests, whereas methylene-bis-acrylamide exhibited the highest general cytotoxicity, in terms of chromium release.…”

Section: Discussionmentioning

confidence: 99%

Acrylamide and Glycidamide Impair Neurite Outgrowth in Differentiating N1E.115 Neuroblastoma Without Disturbing Rapid Bidirectional Transport of Organelles Observed by Video Microscopy

Brat¹,

Brimijoin²

1993

Journal of Neurochemistry

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The nature of the pathogenic insult in acrylamide neuropathy is unknown, but axonal transport disturbances are suspected. Using N1E.115 neuroblastoma in vitro, we examined acrylamide and related compounds in terms of general cytotoxicity, ability to block neurite outgrowth, and effects on neurite integrity and fast axonal transport. Acrylamide, glycidamide, and methylene-bis-acrylamide were weakly cytotoxic in a 51Cr-release assay, but only at > or = 10 mM (order of efficacy: methylene-bis-acrylamide > glycidamide > acrylamide). Neurite outgrowth by differentiating cells was inhibited at 100-fold lower concentrations, with similar EC50 values for all three toxicants, i.e., acrylamide, 70 +/- 15 microM; methylene-bis-acrylamide, 92 +/- 31 microM; glycidamide, 120 +/- 30 microM. Only glycidamide (1 mM) caused degeneration of established neurites within a period of 48 h. Video-enhanced contrast differential interference contrast microscopy was used to test the effect of acrylamide and glycidamide on organelle transport in the neurites. In exposures of < or = 48 h at 1 mM, neither toxicant altered bidirectional organelle flux, measured as organelles transported per minute per micrometer of neurite diameter. Anterograde and retrograde organelle speeds were also undisturbed. These results suggest that mechanisms other than direct inhibition of organellar motility are responsible for acrylamide's neurotoxicity in vivo.

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“…Methyl Alcohol was more toxic in NG108-15 cells than in other cells (Xie and Harvey 1993). Koerker, Berlin, and Schneider (1976) added short-chain alcohols, including Methyl Alcohol, and their corresponding aldehydes, including formaldehyde, to cultures of the NBP 2 clone of C1300 mouse neuroblastoma cells to determine the cytotoxicity of the chemicals. The experimental concentrations ranged up to 2 M. Cytotoxicity was determined by making duplicate observations at 2, 12, 24, 48, and 72 hours after exposure: the percentage of cells with "neurite-like" processes, the percentage of cells sloughing in the medium, the total cell number, and the cell viability (as the percentage of cells that excluded 0.1% Trypan blue in phosphate-buffered saline (PBS) after a 2-minute incubation at 37 ± C).…”

Section: Cytotoxic Effectsmentioning

confidence: 99%

Final Report on the Safety Assessment of Methyl Alcohol

Lanigan¹

2001

International Journal of Toxicology

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Methyl Alcohol is an aliphatic alcohol with use in a few cosmetic formulations as a solvent and denaturant. Concentrations up to 5% are typically used to denature ethyl alcohol in cosmetic products. Methyl Alcohol is readily absorbed through the skin and from the gastrointestinal and respiratory tracts, is distributed throughout all organs and tissues (in direct relation to the body's water distribution), and is eliminated primarily via the lungs. Undiluted Methyl Alcohol is an ocular and skin irritant. Inhalation studies showed a no-effect level for maternal damage of 10,000 ppm and for teratogenic effects of 5000 ppm. Overall, Methyl Alcohol is not considered mutagenic. Carcinogenicity data were unavailable. The toxicity of Methyl Alcohol in humans results from the metabolism of the alcohol to formate and formic acid through a formaldehyde intermediate. Formate accumulation causes metabolic acidosis and inhibits cellular respiration. Methyl Alcohol toxicity is time and concentration dependent, and its toxic effect is competitively inhibited with ethyl alcohol. Because of the moderating effect of ethyl alcohol, it was concluded that Methyl Alcohol is safe as used to denature ethyl alcohol used in cosmetic products. No conclusion was reached regarding any other use of Methyl Alcohol.Methyl Alcohol is readily absorbed through the skin and from the gastrointestinal and respiratory tracts, and distribution

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The cytotoxicity of short-chain alcohols and aldehydes in cultured neuroblastoma cells

Cited by 29 publications

References 9 publications

Ethanol Induces Cell Death and Cell Cycle Delay in Cultures of Pheochromocytoma PC12 Cells

Ethanol Induces Cell Death and Cell Cycle Delay in Cultures of Pheochromocytoma PC12 Cells

Acrylamide and Glycidamide Impair Neurite Outgrowth in Differentiating N1E.115 Neuroblastoma Without Disturbing Rapid Bidirectional Transport of Organelles Observed by Video Microscopy

Final Report on the Safety Assessment of Methyl Alcohol

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