Reference

State of the placenta under the effect of some environmental factors

State of the placenta under the effect of some environmental factors. Barilyak, I. R. (Kiev Res. Inst. Pediatr., Obstet. Ginecol., Kiev, USSR). Pediatr., Akush. Ginekol., (6), 46-8 (Ukrainian) 1977. CODEN: PDAGA2. ISSN: 0031-4048. DOCUMENT TYPE: Journal CA Section: 4 (Toxicology) A single administration of chloridin (I) [58-14-0], 2-(b-ethylaminoethyl)pyridine-HCl (II) [67085-10-3], 6-mercaptopurine (III) [50-44-2], 2-mercaptobenzimidazole (IV) [583-39-1], actinomycin D (V) [50-76-0], or pentoxyl (VI) [147-61-5] to rats on day 13 of gestation caused mortality of 24.7, 29.8, 12.6, 28.0, 18.2, and 13.4% of embryos, resp., as compared to 4.7% postimplantation mortality in controls. Chronic hypobaric hypoxia during 20 days of pregnancy caused 77.4% fetal mortality. I, III, II, and hypoxia induced teratogenesis in 100, 100, 3.8, and 9.4% of the embryos, resp. I, and to a smaller extent also II and III induced hypervolemia of placental blood vessels, accumulation of leuko- and lymphocytes, and increased the vol. of nuclei in the symplastic cells of the placenta. VI at 500 mg/kg caused hypertrophy of symplastic cells of the fetal portion of the placenta and increased the nucleus vol.. IV caused extensive hemorrhages in the uteral portion of the placenta, homogenization of the walls of blood vessels, and pyknosis of endothelial nuclei. V caused extension of lacunae, local hemorrhages, accumulation of leukocytes in the luman of the lacunae, and hypertropy of the nuclei of symplastic cells. Hypoxia caused either necrosis or extensive hemorrhages in the placenta. IV and V caused the greatest changes in the morphol. of large placental arteries.

Genetic evidence for physical interactions between enzymes of nucleotide synthesis and proteins involved in DNA replication in bacteriophage T4

Genetic evidence for physical interactions between enzymes of nucleotide synthesis and proteins involved in DNA replication in bacteriophage T4. Macdonald, Paul M.; Hall, Dwight H. (Sch. Appl. Biol., Georgia Inst. Technol., Atlanta, GA 30332, USA). Genetics, 107(3), 343-53 (English) 1984. CODEN: GENTAE. ISSN: 0016-6731. DOCUMENT TYPE: Journal CA Section: 3 (Biochemical Genetics) Mutations in phage T4 genes 41 (5 of 5) and 61 (3 of 3) cause resistance to the folate analog pyrimethamine [58-14-0] that inhibits T4 dihydrofolate reductase [9002-03-3]. These genes code for subunits of a T4 primase [64885-96-7] and are part of a putative T4 replication complex. In contrast with many previously isolated folate analog-resistant (Far) T4 mutants, these T4 primase mutants do not overproduce dihydrofolate (FH2) reductase nor do they alter its primary structure. A new mutant with a single lesion in gene 41 was isolated which proved resistant to the folate analog at 30° and was lethal at 42°. This mutant induced normal levels of FH2 reductase (encoded by the frd gene) and appeared to have normal expression of other T4 genes at 30°. Like other mutations in gene 41, tsP129 reduced phage-induced DNA synthesis to ~15% that of wild-type T4, as measured by thymidine incorporation under restrictive conditions. Double mutants carrying mutations in genes 41 and 61, 41 and frd or 61 and frd showed allele-specific suppression which suggests that the products of these genes interact. Apparently, abnormal interactions between components of the replication complex and a DNA precursor-synthesizing complex cause folate analog resistance by allosterically altering the T4 FH2 reductase.