The postnatal pattern of ornithine decarboxylase activity reveals a disparity of rat brain regeneration capacity after prenatal X-ray or 5-azacytidine treatment.
Pregnant Wistar rats were treated on the 15th day of gestation either with 1.4 Gy X-radiation, or with 2 X 2.5 mg 5-azacytidine per kg body weight. X-irradiation caused negligible mortality among the offspring, despite of a 35% reduction of brain weights. The course of brain ornithine decarboxylase activity exhibited two breaches within 5 days after birth, each followed by recovery to control levels. After 5-azacytidine treatment brain weights were reduced by 16% only, but two thirds of the young died within a short time after birth. During three days following birth, the activity of ornithine decarboxylase in the brains of the young animals split into two ranges, a high one at control level and a low one at about one fifth of control level. As the ratio of brains with low to those with high enzyme activities correlated with the rate of postnatal mortality, the splitting of early postnatal enzyme activities was interpreted in terms of a nothing-or-all-law: beyond a certain amount of 5-azacytidine incorporated into brain DNA, gene expression was impaired to an extent not compatible with the survival of the animals.
D000818:Animals; D001374:Azacitidine / Q000633:toxicity*; D001921:Brain / Q000201:enzymology* / Q000502:physiology / Q000528:radiation effects; D005260:Female; D009929:Organ Size / Q000187:drug effects / Q000528:radiation effects; D009955:Ornithine Decarboxylase / Q000378:metabolism*; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D011919:Rats, Inbred Strains; D012038:Regeneration
D009955:Ornithine Decarboxylase; D001374:Azacitidine