Characterization of RNA from equine infectious anemia virus.

The genome of equine infectious anemia virus, a nononcogenic retrovirus, has been characterized by velocity sedimentation, electrophoresis in polyacrylamide gels, buoyant density in CS2SO4, and susceptibility to nuclease digestion. The nucleic acid of purified virus was resolved by sedimentation analysis into a fast-sedimenting genome component, which comprises about two-thirds of the virion RNA, and a slow-sedimenting RNA, which is probably comprised of host-derived tRNA and a trace amount of 5S RNA. The fast-sedimenting RNA had a sedimentation coefficient of 62S and a molecular weight of 5.4 X 10(6) to 5.6 X 10(6), as determined by sedimentation velocity and electrophoretic mobility. Upon heat denaturation, [3H]uridine-labeled 62S RNA dissociated into material comprised of 90 to 95% single-stranded species, sedimenting predominantly at 34S, with a molecular weight of 2.7 X 10(6) to 2.9 X 10(6) and 5 to 10% 4S RNA. The 62S RNA was predominantly single-stranded but contained double-stranded regions, as indicated by partial resistance to RNase IA and SI nuclease and by a lower buoyant density in CS2SO4 than that of the single-stranded 34S RNA derived by heat denaturation. These data indicated that the viral genome consisted of two 34S subunits of single-stranded RNA held in a high-molecular-weight complex with 4S RNA by a mechanism involving a small degree of base pairing. Thus, the structure of equine infectious anemia virus RNA is similar to that of other retroviruses.     

Growth of cultured cells from patients with Fanconi anemia.

Fibroblast cultures derived from skin biopsies of patients with Fanconi anemia had doubling times (mean of five lines: 30.3 +/- 0.2 hours) significantly longer than randomly selected normal controls (mean of nine lines: 22.9 +/- 0.4 hours). Control cultures grew more slowly in the enriched media RPMI 1640 and McCoy's 5A than in MEM; while a culture from a patient with Fanconi anemia grew more slowly only in McCoy's 5A. Differences in growth characteristics between Fanconi anemia and normal cell cultures may be useful in analyzing the metabolic error determined by the Fanconi anemia gene.     

Ochratoxin A-induced iron deficiency anemia.

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.     

Ochratoxin A-induced iron deficiency anemia.

Ochratoxin A at 8 micrograms per g of diet, but not at lower doses, fed to chickens from 1 day to 3 weeks of age resulted in significantly (P less than 0.05) decreased packed blood cell volume and hemoglobin concentration without altering the number of circulating erythrocytes. Serum iron and percentage of transferrin saturation were lowered at 4 and 8 micrograms/g. Therefore, anemia was characteristic of severe ochratoxicosis of young chickens, and the anemia was categorized as a hypochromic-microcytic anemia of the iron deficiency type. These data indicate that ochratoxin A by itself does not cause hemorrhagic anemia syndrome of chickens and that an anemia caused by a nutritional deficiency can be elicited by a mycotoxin.     

Effects of alkylating agents on lymphocytes from controls and from patients with Fanconi's anemia

Summary The frequency of sister chromatid exchanges (SCE) and chromosome aberrations and the dynamics of cell division in peripheral blood lymphocytes of four patients with Fanconi's anemia were studied after in vitro exposure to alkylating agents TEPA and mitomycin.SCE frequency was significantly increased even after very low doses of mutagens, while chromosome aberrations were significantly increased only after high doses (0.160 g/ml mitomycin and 10^-5 M TEPA). The responses of Fanconi's anemia cells and control cells did not differ significantly. The increased frequency of both SCE and chromosome aberrations was accompanied by gradual delay of cell division, which was most conspicuous in cells from patients with Fanconi's anemia.