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Haasch ML, Ford AW: Combined effects of ethanol and cinnamaldehyde in the Japanese medaka embryo-larval assay (MELA). Mar Environ Res. 2004 Aug-Dec;58(2-5):175-9.
The Japanese medaka (Oryzias latipes) was used in the medaka embryo-larval assay (MELA) to determine possible adverse developmental effects of ethanol and the spice component, cinnamaldehyde (CAD). Fish may be exposed to waterborne ethanol and a variety of natural products from non-point sources or leaks during ethanol use as a fuel and from point source processing plant effluents. Consumption of ethanol during human pregnancy is known to cause fetal alcohol syndrome (FAS), a collection of birth defects including craniofacial abnormalities thought to be caused by the generation of free radicals during ethanol metabolism by both alcohol and aldehyde dehydrogenase (s). Fish are also susceptible to FAS (Dasmahapatra et al., meeting abstract). The activity of aldehyde dehydrogenase is inhibited by CAD [Biochem. J. 282 (1992) 353-360; Biochem. Pharmacol. 45 (1993) 1621-1630], and CAD is known to cause developmental abnormalities in the rat [Food Chem. Toxicol. 27 (1989) 781-786]. Therefore, the combined effects of treatment with both ethanol and CAD would be expected to produce additive or greater than additive effects in the MELA assay. Medaka were exposed to ethanol at 100 mM, CAD at 10, 1.0, 0.67 or 0.50 mM, to ethanol and CAD combined, or were non-treated controls. Ethanol at 100 mM was without effect. CAD alone at 10 mM and 1.0 mM was lethal by 1 dpf. Embryos exposed to 100 mM ethanol and 0.67 mM CAD exhibited cardiovascular and pigmentation defects and delayed hatching. Embryos exposed to 0.50 mM CAD alone had less severe cardiovascular problems as compared to the combined ethanol and CAD treatment. Taken together the results indicate that the combined effects of ethanol and CAD are greater than the individual effects and indicate the need to monitor effluents in fish nursery areas to protect natural fish populations. Supported by PHS/NIH ES07929. |
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