Subacute ethanol consumption reverses p-xylene-induced decreases in axonal transport.
Human exposure to organic solvents is often complicated by ethanol ingestion and the literature is replete with demonstrations of metabolic interactions between ethanol and organic solvents at a pharmacokinetic level. Because of the possible modulation of xylene toxicity by ethanol consumption, the present group of studies characterizes the effect of ethanol on the p-xylene-induced decrease in axonal transport in the rat optic system previously reported by our laboratory. Long-Evans, hooded, male rats were divided randomly into two groups: those receiving 10% ethanol in their drinking water and those receiving water only. These two groups were further subdivided into two groups which were either exposed by inhalation to 1600 ppm p-xylene for 6 h/day, 5 days/week for 8 exposure-days or were treated identically except that they were exposed to air while in the inhalation chambers. The ethanol-drinking rats were given ethanol 6 days prior to and on the days of the inhalation exposure. Immediately after removal from the inhalation chambers on the last exposure day, the animals were injected intraocularly with [35S]methionine and [3H]fucose to measure the synthesis and rapid axonal transport of proteins and glycoproteins, respectively, in the retinal ganglion cells. The animals were sacrificed 20 h later, and the amount of radioactivity in different areas of the retinal ganglion cells was determined by liquid scintillation counting. As in previous experiments, the xylene exposure group showed a significant reduction in axonal transport of proteins and glycoproteins, whereas the ethanol exposure alone produced no significant reductions in the transport of either proteins or glycoproteins. In the animals receiving both ethanol and xylene, however, the ethanol treatment prevented the decreased transport characteristic of the xylene only animals, i.e. in all areas of the optic projections the level of transport were similar to the level present in the control groups. These data suggest that the xylene-induced reduction in rapid axonal transport was reversed (or prevented) by subacute ethanol consumption.
D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D001370:Axonal Transport / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D000431:Ethanol / Q000633:toxicity*; D005123:Eye / Q000187:drug effects / Q000378:metabolism; D005136:Eye Proteins / Q000096:biosynthesis / Q000378:metabolism; D006023:Glycoproteins / Q000096:biosynthesis / Q000378:metabolism; D008297:Male; D008715:Methionine / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012160:Retina / Q000187:drug effects / Q000378:metabolism; D013462:Sulfur Radioisotopes; D014316:Tritium; D014992:Xylenes / Q000633:toxicity*
D005136:Eye Proteins; D006023:Glycoproteins; D013462:Sulfur Radioisotopes; D014992:Xylenes; D014316:Tritium; D000431:Ethanol; C031286:4-xylene; D008715:Methionine