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Biomedical subjects

A Russo

Publications and source records attributed to A Russo.

At least 649 records · Page 36Linked to original sources
PubMed1983

Bromodeoxyuridine in tumors and chromosomes detected with a monoclonal antibody.

Using a monoclonal antibody to bromodeoxyuridine (BUdR) and immunohistochemistry, we measured the incorporation of this thymidine analogue into the DNA of human normal and malignant cells exposed in vivo. BUdR given as a constant intravenous infusion for 12 or 24 h daily for up to 13 d resulted in a steady-state plasma level of 10(-6) M during the infusion. We demonstrated extensive incorporation of BUdR into both normal skin, normal bone marrow, and malignant melanoma cells. In addition, this infusion of BUdR was adequate to identify sister chromatid exchanges from human marrow chromosomes exposed in vivo. Using this constant infusion, significant but reversible (acute) toxicity was observed with myelosuppression and skin photosensitivity. These techniques, which are considerably less cumbersome and time-consuming than the use of radioactive isotopes of thymidine, can be used for further human studies of cell kinetics and chromosomal replication in both normal and malignant cells.

Animals↗
PubMed1983

Thiols, thiol depletion, and thermosensitivity.

Hyperthermia sensitization or tolerance is subject to cellular events that may occur at membrane, nuclear, and cytoplasmic sites. We have studied the effects of elevated temperatures on the oxidative-reductive state of the cell by measuring and altering glutathione (GSH) concentrations. GSH plays a pivotal role in maintaining the overall cellular redox state and detoxification of peroxides. Continuous heating at 42.5 degrees C or acute exposure at 43 degrees C or 45.5 degrees C resulted in rapid elevations of cellular GSH to 120-200% of control values. Qualitatively, the more severe the heat exposure, the quicker the maximal GSH levels are attained. Ethanol, a compound that also induces thermal tolerance, likewise increases intracellular GSH concentrations. GSH depletion by two different modalities, diethylmaleate (DEM) and buthionine sulfoximine (BSO), results in thermal sensitization. It was demonstrated that once thermotolerance has been induced, depletion of GSH has minimal effects on subsequent heating and thermotolerance. Heat shock protein (HSP) synthesis is lessened by treatment with buthionine sulfoximine; the extent of the decrease in HSP production correlates with the decrease in thermotolerance. The exogenous thiol cysteine combined with heat treatment results in thermosensitization. Exogenous cysteine is found to oxidize to cysteine and to enhance oxygen consumption. The use of N-acetylcysteine resulted in less oxygen consumption and less thermosensitization. A proposed mechanism of peroxide-induced cell damage is suggested by exogenous thiols, as well as an involvement of GSH in the initial aspects of thermotolerance induction.

Acetylcysteine↗
PubMed1983

A new rare variant of the glyoxalase I system of the red cell: GLO-Sicily.

A fast variant of the red cell enzyme glyoxalase I was identified in a sample of 663 persons from Eastern Sicily; the allele was designated GLOSi. The gene frequencies for the common alleles GLO1 and GLO2 are not different from those observed in other southern Italian populations, and are in agreement with the hypothesis of a westward gene flow from Asia.

Alleles↗
PubMed1983

Cellular glutathione depletion by diethyl maleate or buthionine sulfoximine: no effect of glutathione depletion on the oxygen enhancement ratio.

The hypoxic and euoxic radiation response for Chinese hamster lung and A549 human lung carcinoma cells was obtained under conditions where their nonprotein thiols, consisting primarily of glutathione (GSH), were depleted by different mechanisms. The GSH conjugating reagent diethylmaleate (DEM) was compared to DL-buthionine-S,R-sulfoximine (BSO), an inhibitor of glutathionine biosynthesis. Each reagent depleted cellular GSH to less than 5% of control values. A 2-hr exposure to 0.5 mM DEM or a 4- or 24-hr exposure to BSO at 10 or 1 mM, respectively, depleted cellular GSH to less than 5% of control values. Both agents sensitized cells irradiated under air or hypoxic conditions. When GSH levels are lowered to less than 5% by both agents, hypoxic DEM-treated cells exhibited slightly greater X-ray sensitization than hypoxic BSO-treated cells. The D0's for hypoxic survival curves were as follows: control, 4.87 Gy; DEM, 3.22 Gy; and BSO, 4.30 Gy for the V79 cells and 5.00 Gy versus 4.02 Gy for BSO-treated A549 cells. The D0's for aerobic V79 cells were 1.70 Gy versus 1.13 Gy, DEM, and 1.43 Gy for BSO-treated cells. The D0's for the aerobic A549 were 1.70 and 1.20 for BSO-treated cells. The aerobic and anoxic sensitization of the cells results in the OER's of 2.8 and 3.0 for the DEM- and BSO-treated cells compared to 2.9 for the V79 control A549. BSO-treated cells showed an OER of 3.3 versus 3 for the control. Our results suggest that GSH depletion by either BSO or DEM sensitizes aerobic cells to radiation but does not appreciably alter the OER.

Animals↗
PubMed1983

Glutathione elevation during thermotolerance induction and thermosensitization by glutathione depletion.

Chinese hamster V79 cells were made thermotolerant by either continuous heating at 42.5 degrees or by fractionated 43 degrees exposures with interfraction incubation at 37 degrees. For both methods of thermotolerance induction, elevations in cellular glutathione (GSH) were observed. Additionally, GSH was also shown to be elevated following a 1-hr exposure to 6% ethanol, which also induces thermotolerance. These elevations in cellular GSH preceded thermotolerance induction in regard to cell survival. To determine if a reduction in cellular GSH prior to or during heating at 42.5 degrees would influence thermotolerance, GSH levels were reduced by either pretreatment with diethylmaleate, an agent that binds GSH, or treatment during heating with buthionine sulfoximine, an agent that inhibits GSH synthesis. Both depleting protocols resulted in thermosensitization. These data suggest that GSH may be important in the early cellular response to thermal stress.

Animals↗
PubMed1982

[Injections of peroxidase in the ventrobasal complex of the amygdala: afferent connections].

The relationships between the ventrobasal (VB) complex of the amygdala and the other encephalic zones have been investigated. Horseradish peroxidase injections were made into the amygdaloid VB complex in seven adult rats, processed according to the Nauta method (2). HRP labelled somata were observed ipsi- and contralaterally into the lateral habenulae (HL), superior collicoli (CS), reticular formations (RF), dorsal and medial raphe nuclei (DR and MR), only contralaterally into bulbar dorsal vagal nucleus (NDV) Fig. 1).

Amygdala↗
PubMed1981

[Determination of lactic dehydrogenase isoenzymes in precancerous and cancerous gastric mucosa].

We have studied modifications of LDH isoenzymes pattern in normal human gastric mucosa as well as in adenocarcinoma and precancerous lesions of the stomac (gastritis and ulcer); samples from the injured and the surrounding non-injured area were examined, drawing up the isoenzymes, using Tris-buffer pH 7,4 at 4 degrees C and performing the determination within 1 h - because of the high chronolability of the fractions LDH and LDH by cellogol electrophoresis separation. We have always noticed - especially in samples from adenocarcinoma- a shifting toward the M chains, with a clear increase of the fractions LDH4 and LDH5; this has been noticed even in the surrounding non-injured area.

Adenocarcinoma↗
PubMed1981

[Afferent and efferent connections between the hypothalamus and raphe. Study using the technic of retrograde transport of peroxidases].

Projections between rat lateral hypothalamus and dorsal and medial raphe nuclei were studied. Horse radish peroxidase (HRP) was injected into each of these structures and retrogradely labeled neurons were identified. Following HRP injections into lateral hypothalamus (LH) labeled neurons were found into medial and cortical amygdaloid nuclei (AME, ACO), into dorsal thalamic nucleus (MD), in the hippocampal gyrus (HPC) and into medial raphe nucleus (MR). Following HRP injections into medial (MR) and dorsal (DR) raphe nuclei, labeled neurons were found in medial, lateral and posterior hypothalamus. A functional circuit was supposed between midbrain raphe and hypothalamus.

Animals↗