Sequential staining with a counterstain-contrasted fluorescent banding technique (chromomycin A3-distamycin A-DAPI) revealed the occurrence of distamycin A-4,6-diamidino-2-phenylindole (DA-DAPI) staining heterochromatin in the centromeric regions of chromosomes 33, 36, 37, and 38 in the wolf (Canis lupus pallipes) and of chromosomes 13, 16, and 23 in the blue fox (Alopex lagopus). The red fox (Vulpes vulpes) lacked such regions. Staining with DAPI--actinomycin D produced a QFH-type banding pattern with clearcut differences in the staining behaviour of DA-DAPI positive regions between these three canid species. Staining with the fluorochrome D 287/170 did not preferentially highlight any of the DA-DAPI positive regions in any of them. Counterstain-enhanced chromomycin A3 R-banding and studies of nucleolus organizer region location and activity confirmed a close relationship between the karyotype of the wolf and the domestic dog. Few heterochromatic marker bands were encountered in these two species, but heterochromatin polymorphism was evident in the blue fox.
Individual and racial differences in response to alcohol and with respect to alcoholism have strong genetic predispositions. Most studies on the actual genetic determinants have concentrated on the isozymes of alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH), the two enzymes of the primary pathway of alcohol metabolism. Although few "activity" variants (associated with mutations in the structural genes) of the two enzymes are known to exist in susceptible groups, these observations do not offer an adequate explanation for the observed variability in response to alcohols in the population. Some recent studies have reported alterations in the specific activity of the two enzymes following exposure to alcohol for different lengths of time in man, rat, and mice. The induction-repression so observed is hypothesized to be regulated by one or more inducibility genetic elements (IGE) associated with the structural loci of the two enzymes. Variability in IGE will permit a genotype (individual) specific response in ADH and ALDH specific activity when challenged with a given level of alcohol. Considering the relative toxicity of acetaldehyde, the primary metabolite of this pathway, the resistant individuals would be expected to show ALDH induction. Conversely, the susceptible individuals should respond to alcohol by ALDH repression. The ability of an individual to show induction or repression following alcohol ingestion will depend on his or her IGE genotype(s) associated with specific enzyme loci. Also, the degree of polymorphism at these loci would be expected to be extensive and yet population and race specific. Once experimentally established, this approach could have important implications in screening, counselling, prevention, and in novel approaches to treatment.
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