Membrane-bound oxygen reductases of the anaerobic sulfate-reducing Desulfovibrio vulgaris Hildenborough: roles in oxygen defence and electron link with periplasmic hydrogen oxidation.

Cytoplasmic membranes of the strictly anaerobic sulfate-reducing bacterium Desulfovibrio vulgaris Hildenborough contain two terminal oxygen reductases, a bd quinol oxidase and a cc(b/o)o3 cytochrome oxidase (Cox). Viability assays pointed out that single Δbd, Δcox and double ΔbdΔcox deletion mutant strains were more sensitive to oxygen exposure than the WT strain, showing the involvement of these oxygen reductases in the detoxification of oxygen. The Δcox strain was slightly more sensitive than the Δbd strain, pointing to the importance of the cc(b/o)o3 cytochrome oxidase in oxygen protection. Decreased O2 reduction rates were measured in mutant cells and membranes using lactate, NADH, ubiquinol and menadiol as substrates. The affinity for oxygen measured with the bd quinol oxidase (Km, 300 nM) was higher than that of the cc(b/o)o3 cytochrome oxidase (Km, 620 nM). The total membrane activity of the bd quinol oxidase was higher than that of the cytochrome oxidase activity in line with the higher expression of the bd oxidase genes. In addition, analysis of the ΔbdΔcox mutant strain indicated the presence of at least one O2-scavenging membrane-bound system able to reduce O2 with menaquinol as electron donor with an O2 affinity that was two orders of magnitude lower than that of the bd quinol oxidase. The lower O2 reductase activity in mutant cells with hydrogen as electron donor and the use of specific inhibitors indicated an electron transfer link between periplasmic H2 oxidation and membrane-bound oxygen reduction via the menaquinol pool. This linkage is crucial in defence of the strictly anaerobic bacterium Desulfovibrio against oxygen stress.

Axial heterogeneity of organic cation transport along the rabbit renal proximal tubule: studies with brush-border membrane vesicles.

Brush-border membrane vesicles prepared from rabbit kidney outer cortex (rich in S1 and S2) and outer medulla (rich in S3) were used to evaluate the axial heterogeneity of tetraethylammonium transport in the proximal tubule. The vesicle preparations had similar Km values but the Vmax values differed, suggesting that axial heterogeneity of tetraethylammonium secretion may be due to differences in transport across the brush-border membrane.

The renal effects of clonidine in unanesthetized rats.

Clonidine s.c. (0.01-0.3 mg/kg), in unanesthetized rats, caused an initial rise (+20 mm Hg), followed by a continuous fall of BP and a dose-dependent natriuresis and diuresis for up to 2 h. Glomerular filtration rate (GFR) (CIn) increased during the first 20 min, while effective renal plasma flow (ERPF) (CPAH) remained normal. Subsequently, between 20 and 60 min after injection, ERPF (CPAH) decreased considerably while GFR had reverted to its normal value. In saline-infused rats clonidine diuresis was accompanied by an "inappropriate" positive free water clearance. Pentobarbital anesthesia suppressed the initial BP peak and the diuresis. Phenoxybenzamine (1 mg/kg i.v.) was antinatriuretic in saline diuresis; the effect of phenoxybenzamine + clonidine on diuresis and salt excretion represented the sum of the effects of both drugs, but phenoxybenzamine enhanced the clonidine-induced increase of GFR. Neither haloperidol (1 mg/kg i.v.) nor bulbocapnine (3 mg/kg i.v.) interfered with the renal effects of clonidine. Clonidine s.c. caused hyperglycemia and glucosuria which did not account for the natriuresis. Clonidine thus appears to increase the GFR and "filtration fraction" (FF) by a phenoxybenzamine-insensitive rise of glomerular ultrafiltration, to depress ERPF by alpha-adrenergic afferent vasoconstriction, to induce natriuresis by a tubular action not blocked by phenoxybenzamine and to exert an antivasopressin effect, either by depressing pituitary vasopressin secretion or the renal response to vasopressin.

[Goldenhar syndrome. Oculoauriculovertebral dysplasia. 2 new pediatric cases]. / Syndrome de Goldenhar. Dysplasie oculo-auriculo-vertébrale. Deux nouvelles observations pédiatriques.

The authors report two new cases of Goldenhar's syndrome, as they are described in Gorlin's scheme of oculo-auriculo-vertebral dysplasia. Therapeutical problems (plastic and orthopedic surgery, ocular prothesis and hearing aid) due to Goldenhar's syndrome are very acutely pointed out in these cases. Generalized convulsions, not yet described in the medical literature, are found in these two cases. These congenital malformations are caused by branchial arches organogenesis anomalies. The authors consider that accurate and early dermatologic diagnosis is important for the correct management of children with oculo-auriculo-dysplasia.

[Herpes and skin lesions: what's new?]. / Herpès et lésions cutanées: quoi de neuf?

The spectrum of clinical lesions of herpes has grown, since the research of viruses by PCR permitted to bind to their etiology discrete or atypical lesions, and even, to display periods of asymptomatic viral excretion. These variable clinical aspects depend on the balance between, on the one hand, the qualitative and quantitative virulence of HSV and, on the other hand, the quality of the immunological defenses of the patient. So, "herpetic primary infection" and "herpetic recurrences" are serological definitions; the clinical aspects of the different stages can be interchangeable. Cultures or PCR and type-specific serologies also showed the increased frequency of HSV1 in genitals, explained by the increased oro-genital sex, since the beginning of AIDS.

[Cytogenetic and cytometric characteristics of cutaneous T-cell lymphomas]. / Caractéristiques cytogénétiques et cytométriques des lymphomes T à expression cutanée.

Evidence from cytogenetic (karyotype) and cytometric studies in cutaneous T-cell lymphomas reported in the medical literature is reviewed. Such studies are still very scarce because of the technical difficulties which arise in culturing the cells. Automatic analysis of chromatin dispersion (flow cytometry) is currently the most promising technique.

Renal transport of organic anions.

This review deals with the different transport mechanisms mediating the apical and basolateral transport of organic anions, all of which are restricted to the proximal tubule. Several transport mechanisms, such as the para-aminohippurate basolateral transporter and the apical proton coupled di- and tripeptide transporter have been cloned, and their role in renal transport has been well characterized. Other transport proteins have been cloned from the kidney, liver, or intestine, but their role in the renal transport of organic anions needs to be elucidated. This is the case with Mdr2, oatp1 and OAT-K1, which were identified in the apical membrane of the proximal tubule, and with MDR1, the precise localization of which is still uncertain. Other apical transport mechanisms, sodium coupled transports and anion exchangers are involved in organic anion reabsorption.

Transport and metabolism of [3H]morphine in isolated, nonperfused proximal tubular segments of the rabbit kidney.

Proximal tubular segments (S1, S2 and S3) of the rabbit kidney were incubated in oxygenated Ringer's solution (30 min, pH 7.4, 37 degrees C) containing bovine serum albumin (10 g/l) and [3H]morphine (0.7 microM). The uptake, expressed as tissue water/medium ratio at equilibrium, for S1 was 42.2 +/- 3.95 (mean +/- S.E.), n = 16 tubules from six animals; for S2, 41.6 +/- 4.17, n = 18 tubules from six animals; and for S3, 29.0 +/- 3.83, n = 15 tubules from six animals, a value significantly lower (P less than .05) than in the S1 and S2 segment. High-performance liquid chromatography analysis of the accumulated tritium revealed metabolism of [3H]morphine. Unchanged morphine represented 35.5 +/- 3.4% of the total radioactivity recovered in the extract from S1 segments, 51.1 +/- 7.7% from S2 and 77.3 +/- 1.8 from S3 segments. After treating the tubular extracts with beta-glucuronidase (5 hr, 25 degrees C), all the recovered radioactivity represented unchanged morphine. The main metabolite, thus, was a glucuronide. KCN (10(-2) M), mepiperphenidol (Darstine, 10(-4) M) and quinine (10(-4) M) inhibited [3H]morphine uptake by 55-70%. Surprisingly, there was no decrease in uptake in the presence of N1-methylnicotinamide (10(-3) M). We conclude that the whole proximal tubule is able to accumulate morphine by a specific transport system for organic cations, but that part of this uptake might be due to cellular metabolism and intracellular binding of the drug.

Transport of salicylate in proximal tubule (S2 segment) isolated from rabbit kidney.

The secretory and reabsorptive transport of salicylate was studied in the isolated and perfused rabbit proximal tubule (S2 segment). Salicylate secretion (Jb----lsal) fulfilled the criteria for a carrier-mediated transport system: Jb----lsal was saturable, was reversibly inhibited by probenecid, and occurred against a concentration gradient. The Km and Vmax for this secretory transport were 80 microM and 3,200 fmol.min-1.mm-1, respectively. At luminal pH of 7.4 and 6.6, salicylate reabsorption (Jl----bsal) was low (100 fmol.min-1.mm-1). Jl----bsal was stimulated by increasing the bath PCO2 or by removing basolateral HCO3-; Jl----bsal was inhibited by ethoxyzolamide and by SITS in the bath. Our results indicate that salicylate reabsorption depends on H+ secretion, consistent with reabsorption by simple nonionic diffusion. When salicylate was present in the lumen only, Jl----bsal increased after inhibition of the secretory transport by adding ouabain or probenecid in the bath or by lowering the bath temperature. These results are compatible with luminal recycling of salicylate, and suggest the presence of a mediated secretory transporter located at the luminal membrane.

Indirect Na+ dependency of urate and p-aminohippurate transport in pig basolateral membrane vesicles.

Membrane vesicles were used to study the basolateral transport of urate and p-aminohippurate (PAH) in the proximal tubule of the pig kidney. Consistent with a cooperation between a Na(+)-2-oxoglutarate cotransporter and a 2-oxoglutarate-urate or a 2-oxoglutarate-PAH exchanger, urate and PAH uptakes were stimulated in presence of extravesicular 2-oxoglutarate when an inwardly directed Na+ gradient was applied. Both transports exhibited, however, different characteristics. The optimal 2-oxoglutarate concentration for stimulating uptakes was 10 microM for PAH and 150 microM for urate. Extravesicular chloride was required to observe a stimulation of PAH uptake but not of urate uptake. Transports of both PAH and urate exhibited different affinity sequences for various organic anions. Stimulated PAH uptake was inhibited by probenecid greater than cold PAH greater than urate = pyrazinoate greater than lactate, whereas stimulated urate uptake was inhibited by probenecid greater than cold urate greater than PAH and not by pyrazinoate or lactate. These results are consistent with independent transport processes for urate and PAH in pig basolateral membrane vesicles, both being indirectly driven by an inwardly directed Na+ gradient.