Comparative genetics of host response to N-methyl-N'-nitro-N-nitrosoguanidine. II. Inverse relationship between tumor susceptibility and salt-hydrocortisone conditioned acceleration of water turnover in rodents.
The purpose of this study was to investigate the nature of the action of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) as the modulator of gene expression. Practically, both the acceleration of daily liquid consumption following salt-hydrocortisone conditioning (sea water adaptation phenomenon) and the suppressive effect of MNNG on that gene expression were comparatively investigated among Wistar rats of both sexes, Buffalo rats of both sexes and Swiss/ICR mice of both sexes. Results obtained are as follows: 1) the responsiveness to the salt-hydrocortisone conditioning, as assessed in terms of weight-adjusted liquid consumption, decreased in the order of female Swiss mice greater than male Swiss mice greater than Buffalo rats of both sexes greater than female Wistar rats greater than male Wistar rats, a finding which indicates that an inverse relationship exists between the expression of the sea water adaptation gene and that of putative stomach proto-oncogene. 2) Additional MNNG conditioning (provision of MNNG drink) eradicated the accelerating effect of the salt-hydrocortisone conditioning on the water turnover of a rodent. 3) Evidence was presented to indicate that MNNG acted as an antiandrogen in expressing the above effect. In conclusion, our findings are taken as evidence to support the proposition that the sea water adaptation gene and the stomach proto-oncogene compete with each other in the possession of one common MNNG-sensitive (and/or steroid-sensitive) enhancer gene in their gene expressions.
Kodama
M
M
Biophysics Division National Cancer Center Research Institute, Tokyo, Japan.
Inoue
F
F
Kodama
T
T
Kodama
M
M
D000222:Adaptation, Physiological; D000818:Animals; D001834:Body Water / Q000378:metabolism*; D003213:Conditioning, Psychological; D005260:Female; D015870:Gene Expression / Q000187:drug effects*; D006854:Hydrocortisone / Q000494:pharmacology*; D008297:Male; D008769:Methylnitronitrosoguanidine / Q000633:toxicity*; D051379:Mice; D008813:Mice, Inbred ICR; D011519:Proto-Oncogenes; D051381:Rats; D011915:Rats, Inbred BUF; D011919:Rats, Inbred Strains; D012965:Sodium Chloride / Q000494:pharmacology*; D013274:Stomach Neoplasms / Q000139:chemically induced*
D008769:Methylnitronitrosoguanidine; D012965:Sodium Chloride; D006854:Hydrocortisone