Oxidative stress-induced DNA damage and repair in human peripheral blood mononuclear cells: protective role of hemoglobin.

Background: DNA repair is a cellular defence mechanism responding to DNA damage caused in large part by oxidative stress. There is a controversy with regard to the effect of red blood cells on DNA damage and cellular response.

Aim: To investigate the effect of red blood cells on H2O2-induced DNA damage and repair in human peripheral blood mononuclear cells.

Effect of immunosuppressive drugs on spontaneous DNA repair in human peripheral blood mononuclear cells.

Introduction: Immunosuppressive treatment increases the risk of post-transplant cancer. Cyclosporine reduced UV-induced DNA repair by peripheral blood mononuclear cells (PBMC) and increased cancer incidence in kidney transplant recipients. Calcineurin inhibitors (CNI), but not mammalian target of rapamycin (mTOR) inhibitors or mycophenolic acid, suppressed H₂O₂-induced DNA repair in human peripheral blood mononuclear cells (PBMC) in vitro at maintenance drug concentrations.

Effect of immunosuppressive drugs on DNA repair in human peripheral blood mononuclear cells.

Introduction: Cancer is a major cause of mortality among transplant recipients. Immunosuppressive treatment is a modifiable factor contributing to this phenomenon. Cyclosporine in kidney transplant recipients was associated with reduced UV-induced DNA repair by peripheral blood mononuclear cells (PBMC) and increased cancer rate.

Inhibition of mitochondrial function reduces DNA repair in human mononuclear cells.

Background: Mitochondria provide ATP and Ca(2+) needed for DNA repair, but also produce reactive oxygen species (ROS), which may damage DNA.

Aim: To investigate the effect of mitochondrial function inhibition on DNA repair.

Method: Five mitochondrial inhibitors acting at various sites of electron transport were studied.

Spontaneous DNA repair increases during hemodialysis.

Background: Hemodialysis (HD) patients are subjected to increased oxidative stress. Oxidative stress causes DNA damage, which may be repaired by a DNA repair system. 'Spontaneous DNA repair' expresses DNA repair of in vitro unstimulated cells.

Spontaneous DNA repair in human mononuclear cells is calcium-dependent.

Spontaneous DNA repair in peripheral blood mononuclear cells (PBMC) has been recently described. The aim of this study was to evaluate whether spontaneous DNA repair is Ca(2+)-dependent, as in vitro-stimulated DNA repair. Spontaneous DNA repair in PBMC was measured in a 1mM Ca2+ medium.

Spontaneous DNA repair in human peripheral blood mononuclear cells.

DNA molecules are constantly damaged during mitosis and by oxygen-free radicals produced by either cellular metabolism or by external factors. Populations at risk include patients with cancer-prone disease, patients under enhanced oxidative stress, and those treated with immunosuppressive/cytotoxic therapy. The DNA repair process is crucial in maintaining the genomal DNA integrity.

DNA repair in mononuclear cells: role of serine/threonine phosphatases.

Treatment with cyclosporin A (CsA) in kidney-transplant recipients is associated with reduced DNA repair and enhanced cancer incidence. CsA is an inhibitor of the serine/threonine phosphatase calcineurin, also termed PP2B, which is a Ca(2+)/calmodulin-dependent phosphatase. In this study we sought to elucidate the role of calcineurin in DNA repair using CsA and tacrolimus; examine whether UV-induced DNA repair is associated with dephosphorylation; and investigate whether phosphatases other than calcineurin are active in DNA repair, in light of the fact that calcineurin inhibition only partially suppressed DNA repair.

The contribution of an arteriovenous access for hemodialysis to left ventricular hypertrophy.

Background: The long-term isolated contribution of hemodialysis arteriovenous access (AVA) to cardiac hemodynamics has not been previously investigated in a prospective manner.

Methods: Twelve predialysis patients were studied before and 1 and 3 months after creation of a primary AVA. Evaluation included relevant clinical parameters, echocardiographic studies, and hemodynamic hormones.

Effect of cyclosporin A on DNA repair and cancer incidence in kidney transplant recipients.

Cancer incidence is enhanced in transplant recipients. Decreased DNA repair ability is associated with increased cancer incidence. Transplanted patients with cancer were found to have reduced DNA repair.

Haemolysis in haemodialysis patients: evidence for impaired defence mechanisms against oxidative stress.

Background: Uraemic patients have a decreased ability to withstand oxidative stress. It is postulated that their antioxidant capacity is reduced, yet the mechanism remains unclear. Recently 33 haemodialysis (HD) patients were exposed to chloramine contamination in the water supply.

Erythropoietin, folic acid deficiency and hyperhomocysteinemia: is there a possible relationship in chronically hemodialyzed patients?

Aims: To examine the possible relationships between recombinant human erythropoietin (rhEPO) therapy, serum folic acid and homocysteine levels in a cohort of stable, chronically hemodialyzed patients.

Material And Methods: The study was cross-sectional in its first phase and consisted of 3 groups of subjects (group 1:6 healthy controls; group 2:7 dialyzed patients not receiving rhEPO; group 3: 14 patients on rhEPO therapy). Hematological and biochemical parameters were taken after an overnight fast in all subjects.

Lymphocytic intracellular calcium in a patient with complicated verapamil overdose.

Overdose with calcium channel blockers (CCBs) may lead to serious complications. CCBs act by blocking calcium entry into the cell, thus lowering intracellular calcium ([Ca2+]i). [Ca2+]i during CCB overdose has not yet been reported.

Impaired lymphocyte calcium metabolism in end-stage renal disease: enhanced influx, decreased efflux, and reduced response to mitogen.

Lymphocytes from patients with end-stage renal disease (ESRD) exhibit elevated cytosolic calcium concentration ((Ca2+)i), but the mechanisms responsible for this elevated (Ca2+)i have not been entirely elucidated. In addition, lymphocyte proliferative responses to mitogenic stimuli are suppressed in patients with ESRD. The objectives of the study were as follows: (1) to measure calcium influx and efflux in lymphocytes from patients with ESRD; (2) to measure the effect of the calcium regulator parathyroid hormone (PTH) on lymphocyte (Ca2+)i; (3) to measure cytosolic calcium signal in patients' lymphocytes after mitogenic stimulation.

H2O2 induces DNA repair in mononuclear cells: evidence for association with cytosolic Ca2+ fluxes.

Cellular DNA repair systems are induced whenever DNA is damaged. Reactive oxygen species (ROS) are generated, in vivo, in the tissues as a result of regular cellular metabolism or after exposure to oxidizing agents, such as ultraviolet (UV) irradiation. It has been suggested that ROS mediate DNA damage.

The role of calcium in human lymphocyte DNA repair ability.

DNA repair ability is reduced in a variety of pathologic conditions. In addition, in some of these diseases a disturbance in cellular Ca homeostasis occurs or cytosolic (Ca2+) responses to various stimuli are impaired. The leading environmental cause for genomal DNA damage is ultraviolet (UV) irradiation.

Bullous dermatosis of end-stage renal disease: a possible association between abnormal porphyrin metabolism and aluminium.

Background: Bullous dermatosis (BD) is becoming increasingly recognized in patients with end-stage renal disease (ESRD). It is clinically reminiscent of porphyria cutanea tarda, but its detailed pathogenesis remains unclear. Studies have shown increased porphyrin levels in dialysis patients, and this may partly explain the skin lesions and photosensitivity evident in these patients.

DNA repair and recovery of RNA synthesis in uremic patients.

A high frequency of cancer appears among uremic patients. As depressed DNA repair ability is thought to be one of the causes for malignancy in cancer prone diseases, the present study was undertaken to examine DNA repair in uremic patients. Unscheduled DNA repair synthesis in peripheral lymphocytes was measured after both ultraviolet (UV) and gamma irradiations.

Red blood cell calcium level is elevated in women: enhanced calcium influx by estrogens.

Red blood cell (RBC) calcium level had been found to be higher in women than in men. This study was designed to evaluate whether this is a general phenomenon and to elucidate a possible mechanism for a gender-related difference in RBC calcium levels. Differences in RBC calcium levels between women and men were examined in normal subjects, in patients with chronic renal failure (CRF) who were known to have elevated RBC calcium levels, and in female and male rats.

Impaired DNA repair in patients with end-stage renal disease and its improvement with hemodialysis.

DNA repair following ultraviolet (UV)-induced DNA damage is decreased in some cancer-prone diseases. Cancer frequency in end-stage renal disease patients is higher than in the normal population. Therefore, DNA repair from UV-induced damage in lymphocytes was determined in 11 hemodialysis (HD) patients, 11 patients on continuous ambulatory peritoneal dialysis (CAPD), 10 patients with chronic renal failure (CRF) who had not yet been dialyzed and in 12 controls.

Red blood cell calcium level in chronic renal failure: effect of continuous ambulatory peritoneal dialysis.

Red blood cell (RBC) calcium, calcium 45 influx, and calcium extrusion as indicated by Ca-stimulated, Mg-dependent adenosine triphosphatase (CaATPase) was determined in patients with chronic renal failure (CRF), patients with CRF receiving continuous ambulatory peritoneal dialysis (CAPD) treatment, and controls. Cell calcium, which in the controls was 5.5 mumol/L of cells, was elevated in patients with CRF--30.

Red blood cell calcium homeostasis in patients with end-stage renal disease.

Low cell calcium level is essential for preservation of red blood cell (RBC) membrane deformability and survival. RBCs from patients with end-stage renal disease (ESRD) demonstrate reduction in membrane deformability, possibly as a result of increased RBC cellular calcium level. To evaluate calcium homeostasis in RBCs from patients with ESRD, we measured cell calcium level, basal and "calmodulin"-stimulated calcium-stimulated Mg-dependent ATPase (CaATPase) activity, and calcium 45 efflux were measured before and after hemodialysis.

Sialyltransferase activity and sialic acid levels in multiple myeloma and monoclonal gammopathy.

A significant elevation of peripheral blood mononuclear cell sialyltransferase activity (STA) was observed in 14 patients with multiple myeloma (MM), and compared to 7 patients with monoclonal gammopathy of undetermined significance (MGUS) and to 10 controls. Serum sialyltransferase was significant higher in MM patients as compared to controls. It was also higher than in MGUS patients, but the difference here was not statistically significant.

Sialic acid and neuraminidase activity in rat kidneys 6 months after uninephrectomy.

Sialic acid and neuraminidase activity were determined in the cortex of the remnant kidneys of six uninephrectomized rats. As controls served either the kidneys removed at operation or age-matched kidneys from eight sham operated rats. Six months after uninephrectomy the kidneys became hypertrophied and their mean weight was about 40% higher than age-matched kidneys.