No abstract

Methanobacterium thermoautotrophicum grown on mineral medium contains 120 nmol of Coa-(5-hydroxybenzimidazolyi)cobamides (derivaties of factor HI) per g of dry cell mass as the sole cobamide. The bacterium assimilated several corrinoids and bemzinidazole bases during autotrophic growth. The corrinoids were converted into factor Im; however, after three transfers in 5,6-dimethylbenzimidazole (200 uM)-supplemented mineral medium, derivatives of factor III were completely replaced by derivatives of vitamin B12, which is atypical for methanogens. The total cobamide content of these cells and their growth rate were not affected compared with factor I-containing cells. Therefore, the high cobamide content rather than a particular type of cobamide is required for metabolism of methanogens. Derivatives of factor m are not essential cofactors of cobamide-containing enzymes from methanogenic bacteria, but they are the result of a unique biosynthetic ability of these archaebacteria. The cobamide biosynthesis include unspecific enzymes, which made it possible either to convert non-species-derived comnoids into derivatives of factor m or to synthesize other types of cobamides than factor m. The cobamide biosynthesis is regulated by its end product. In addition, the uptake of extracellular cobamides is controlled, and the assimilated corrinoids regulate cellular cobamide biosynthesis. 124 Bq/nmol) in 0.5 ml of 2 M HCl. The solutions were incubated at 130°C for 2 h. After addition of 1 ml of concentration ammonia, the samples were twice flash evaporated to dryness and finally suspended in 500 ,ul of 80% chloroform-20% methanol. The 14C-labeled bases were then 3076 JOURNAL

No abstract

As is known, hypoxia leads to an increase in microcirculatory blood flow of the skin in healthy volunteers. In this pilot study, we investigated microcirculatory blood flow and reactive hyperemia of the skin in healthy subjects in normobaric hypoxia. Furthermore, we examined differences in microcirculation between hypoxic subjects with and without short-term acclimatization, whether or not skin microvasculature can acclimatize. Fourty-six healthy persons were randomly allocated to either short-term acclimatization using intermittent hypoxia for 1 h over 7 days at an FiO2 0.126 (treatment, n = 23) or sham short-term acclimatization for 1 h over 7 days at an FiO2 0.209 (control, n = 23). Measurements were taken in normoxia and at 360 and 720 min during hypoxia (FiO2 0.126). Microcirculatory cutaneous blood flow was assessed with a laser Doppler flowmeter on the forearm. Reactive hyperemia was induced by an ischemic stimulus. Measurements included furthermore hemodynamics, blood gas analyses and blood lactate. Microcirculatory blood flow increased progressively during hypoxia (12.3 ± 7.1–19.0 ± 8.1 perfusion units; p = 0.0002) in all subjects. The magnitude of the reactive hyperemia was diminished during hypoxia (58.2 ± 14.5–40.3 ± 27.4 perfusion units; p = 0.0003). Short-term acclimatization had no effect on microcirculatory blood flow. When testing for a hyperemic response of the skin's microcirculation we found a diminished signal in hypoxia, indicative for a compromised auto-regulative circulatory capacity. Furthermore, hypoxic short-term acclimatization did not affect cutaneous microcirculatory blood flow. Seemingly, circulation of the skin was unable to acclimatize using a week-long short-term acclimatization protocol. A potential limitation of our study may be the 7 days between acclimatization and the experimental test run. However, there is evidence that the hypoxic ventilatory response, an indicator of acclimatization, is increased for 1 week after short-term acclimatization. Then again, 1 week is what one needs to get from home to a location at significant altitude.

No abstract