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Biomedical subjects

M Taber

Publications and source records attributed to M Taber.

4 recordsLinked to original sources

Effects of delipidation on proton translocation and ATPase activity in beef heart electron transport particles.

Delipidation of beef heart electron transport particles with phospholipase A2 has been examined. When the particles were treated with the lipase and subjected to a low bovine serum albumin wash, ATPase activity was unaffected as was the lipid/protein ratio of the particles. However, energisation by ATP/Mg2+ was abolished. Furthermore, unsaturated but not saturated fatty acids discharged the steady-state ATP-driven membrane potential of control samples. When the phospholipase A2 hydrolysis products were removed, inhibition of energy-linked reactions in the lipid-depleted particles was still observed and was interpreted in terms of non-specific leaks in the vesicle membranes, and 'specific' leaks through impaired H+-ATPase complexes. ATPase activity was less susceptible to delipidation than energisation but was, nevertheless, strongly inhibited at 50 percent lipid depletion. Spin label studies indicated a decrease in the fluidity of particle membranes accompanying delipidation. Moreover, the discontinuity seen in Arrhenius plots of ATPase activity was shifted from 17 degrees C (control) to 22 degrees C at 50 percent phospholipid depletion. The data are consistent with a release of unsaturated fatty acids by phospholipase A2 rendering the transport particles both leakier and the membranes less fluid than controls.

Animals

Fluorescent analogues of N,N'-dicyclohexylcarbodiimide as structural probes of the bovine mitochondrial proton channel.

N-Cyclohexyl-N'-[4-(dimethylamino)-alpha-naphthyl]carbodiimide (NCD-4) and N-cyclohexyl-N'-(1-pyrenyl)carbodiimide (NCP) are two novel fluorescent analogues of the mitochondrial inhibitor dicyclohexylcarbodiimide (DCCD). Although nonfluorescent in aqueous media, both compounds form fluorescent conjugates with mitochondrial electron transport particles (ETPH) or purified H+-ATPase (F1-F0) vesicles. DCCD prevents the reaction of ETPH with both NCD-4 and NCP. The fluorescent probes are effective inhibitors of ATPase activity and ATP-driven membrane potential, although their reaction rates are considerably slower than that of DCCD. The fluorescence of NCD-4- or NCP-treated H+-ATPase is quenched by hydrophobic spin-label nitroxide derivatives of stearic acid (chi-NS) in the order 16-NS greater than 12-NS greater than 7-NS approximately equal to 5-NS, whereas membrane-impermeant iodide ions have negligible effect. The quenching behavior of 16-NS (the most effective quencher) suggests that a small fraction of labels remain inaccessible to the quencher. It is concluded that the DCCD-binding sites are oriented toward the membrane lipids and are located in the lipid bilayer ca. 18 A from the membrane surface.

Adenosine Triphosphatases

Association of methemoglobinemia and intravenous nitroglycerin administration.

Significant elevation of arterial methemoglobin levels has been reported with the administration of intravenous (i.v.) nitroglycerin (NTG). To determine the incidence and clinical significance of this side effect of i.v. NTG, serial arterial methemoglobin levels were determined in 50 consecutive patients receiving i.v. NTG for 48 hours or longer. The mean i.v. NTG infusion rate was 290 +/- 13 micrograms/min (4.1 +/- 0.2 micrograms/kg/min) and the mean duration of infusion was 7.1 +/- 0.5 days. The mean methemoglobin level for the 141 samples was 1.57 +/- 0.08%, which differs from the control mean value in our laboratory of 0.44 +/- 0.01%. Although no patient had clinical symptoms from methemoglobin, 20 patients had elevated (greater than 1%) levels on at least 1 measurement. Seventy-eight of the 141 samples analyzed were in the normal range; 63 determinations were between 2 and 5%. Patients with normal methemoglobin levels differed from those with abnormal levels in the dose of i.v. NTG (mean infusion rate 244 +/- 16 vs 351 +/- 17 micrograms/min; total cumulative dose 1,612 +/- 153 vs 3,398 +/- 308 mg). Age, weight, renal and hepatic function, and arterial oxygen saturation were not different between the groups. In conclusion, clinically significant methemoglobinemia is uncommon with i.v. NTG infusion; however, when large doses of NTG are administered, this complication is more likely.

Aged

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Information reported by clients on their previous contacts with community agencies is not accurate. A study of hospital and clinic records indicates that these reports contain omissions significant enough to jeopardize continuity of care.

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