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101.
J. A. Zadunaisky S. Cardona L. Au D. M. Roberts E. Fisher B. Lowenstein E. J. Cragoe Jr. K. R. Spring 《The Journal of membrane biology》1995,143(3):207-217
Transition from low salt water to sea water of the euryhaline fish, Fundulus heteroclitus, involves a rapid signal that induces salt secretion by the gill chloride cells. An increase of 65 mOsm in plasma osmolarity was found during the transition. The isolated, chloridecell-rich opercular epithelium of sea-water-adapted Fundulus exposed to 50 mOsm mannitol on the basolateral side showed a 100% increase in chloride secretion, which was inhibited by bumetanide 10–4
m and 10–4
m DPC (N-Phenylanthranilic acid). No effect of these drugs was found on apical side exposure. A Na+/H+ exchanger, demonstrated by NH4Cl exposure, was inhibited by amiloride and its analogues and stimulated by IBMX, phorbol esters, and epithelial growth factor (EGF). Inhibition of the Na+/H+ exchanger blocks the chloride secretion increase due to basolateral hypertonicity. A Cl–/HCO
3
–
exchanger was also found in the chloride cells, inhibited by 10–4
m DIDS but not involved in the hyperosmotic response. Ca2+ concentration in the medium was critical for the stimulation of Cl– secretion to occur. Chloride cell volume shrinks in response to hypertonicity of the basolateral side in sea-water-adapted operculi; no effect was found on the apical side. Freshwater-adapted fish chloride cells show increased water permeability of the apical side. It is concluded that the rapid signal for adaptation to higher salinities is an increased tonicity of the plasma that induces chloride cell shrinkage, increased chloride secretion with activation of the Na+K+2Cl– cotransporter, the Na+/H+ exchanger and opening of Cl– channels.The work was supported by the National Institutes of Health, Research Grant EYO1340 to J.A.Z. Part of this research was performed while Dr. Zadunaisky was a Scholar In Residence at the Fogarty International Center of The National Institutes of Health in Bethesda, Maryland. Ms. Dawn Roberts was a fellow of the Grass Foundation and Pew Foundation during this work. Grants from the National Science Foundation and the National Institutes of Health to the Mount Desert Island Biological Laboratory also provided assistance for this research. 相似文献
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Non-anemic women attending a public antenatal clinic were given, daily, a multivitamin tablet containing 78 mg. of elemental iron. The follow-up studies included an analysis of their diets. A total of 311 patients were included, of which one group received a supplement of 0.5 mg. folic acid and 0.005 mg. vitamin B12. The incidence of megaloblastic bone marrow change in the unsupplemented group was 26% and of low blood folates approximately 50%. The incidence of megaloblastic changes was sharply reduced in the supplemented group and the blood folates were elevated to supranormal levels, indicating that the dose of folic acid used may have been above the minimal requirement. Formiminoglutamic acid (FIGLU) excretion could not be correlated with other parameters of folate deficiency. Neutrophil lobe counts did not relate to megaloblastic changes or low folate levels unless there was more than 5% hypersegmentation. The dietary intake was suboptimal in total calories, iron and food folate. 相似文献
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105.
Incubation of rat liver mitochondria with 10 microM DL-2-bromooctanoate causes complete and irreversible inactivation of 3-ketothiolase I (acyl-CoA:acetyl-CoA C-acyltransferase). Evidence is presented that mitochondria convert bromooctanoate to 2-bromo-3-ketooctanoyl-CoA, an alpha-haloketone which is probably the active form of the inhibitor. The inactivation is accompanied by incorporation of radioactivity from [1-14C]bromooctanoate into the enzyme. Bromooctanoate does not affect the activities of the other enzymes of beta-oxidation, except for 3-ketothiolase II (acetyl-CoA:acetyl-CoA C-acetyltransferase), which becomes partially inhibited. Evidence is also presented that various enzymes of beta-oxidation can use 2-bromooctanoyl-CoA and its beta-oxidation products as substrates. 相似文献
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Aging exacerbates damage and delays repair of alveolar epithelia following influenza viral pneumonia
Lu Yin Dahai Zheng Gino V Limmon Nicola HN Leung Shuoyu Xu Jagath C Rajapakse Hanry Yu Vincent TK Chow Jianzhu Chen 《Respiratory research》2014,15(1)