Leucocyte volume, conductivity, and scatter at presentation in COVID-19 patients.

Background: In COVID-19 patients, besides changes in leucocyte count, morphological abnormalities of circulating blood cells have been reported. Aim: This study aims to investigate the relationship between the morphological and functional properties of leucocytes and the severity of the disease in COVID-19 patients. Materials and Methods: Blood samples were collected from COVID-19 patients (n = 130) at the time of admission. The patients were stratified according to the comorbidity, age, LDH, lymhocyte count score as mild, moderate, and severe. Complete blood count and the cell population data were analyzed by the Volume, conductivity, scatter (VCS) technology on Beckman Coulter LH-780 hematology analyzer. Kruskal-Wal'lis test was used to assess the differences between the groups with subsequent Bonferroni correction. Results: Neutrophil count was increased, and lymphocyte count was decreased in severe patients compared to mild patients. The increase in the percent of neutrophils and the neutrophil/lymphocyte ratio in the severe patient group was significant in comparison to both the moderate and the mild group. The dispersion of the neutrophil volume and conductivity showed significant changes depending on the severity of the disease. The lymphocyte volume, lymphocyte-volume-SD and lymphocyte-conductivity as well as the monocyte-volume and monocyte-volume-SD were significantly increased in severe patients in comparison to mild patients. The increase of lymphocyte and monocyte volume in severe patients was also significant in comparison to moderate patients. Conclusions: COVID-19 infection leads to important changes in cell population data of leucocytes. The volumetric changes in lymphocytes and monocytes are related to the severity of the disease.

Antithrombin III pretreatment reduces neutrophil recruitment into the lung in a rat model of abdominal sepsis.

BACKGROUND: Antithrombin III (AT III) is a serine protease inhibitor and the mechanism of its anti-inflammatory action is still not understood. In the present study, we aimed to investigate the anti-inflammatory action of AT III on lung injury in a rat model of sepsis. METHODS: Three groups of animals were used in this controlled study: the sham-operated group (sham, n = 3) which only underwent a laparotomy; the control group (control, n = 7) which underwent cecal ligation and perforation (CLP); and the AT III-treated group (AT III, n = 6) which underwent CLP and received intravenous (i.v.) 250 U/kg AT III 30 min before induction of sepsis. Rats were killed 24 h after induction of sepsis by needle aspiration of the right ventricle after a sternotomy, and the lungs and trachea were removed en bloc under ether anesthesia. RESULTS: Pulmonary accumulation of polymorphonuclear leukocytes (PMN) was assessed by measuring lung tissue myeloperoxidase (MPO) activity. Lipid peroxidation in lung tissue was assessed by tissue thiobarbituric acid reactive substance (TBARS) levels. The plasma prostacyclin level was assessed by the plasma 6-keto prostaglandin F(1alpha)(6-keto-PGF(1alpha)) level, which is a stable derivative of prostacyclin. Histopathological changes in lung tissue were assessed by PMN count in the capillaries and alveolar spaces. The lung tissue TBARS level, MPO activity and PMN count in the control group were significantly higher than in the AT III group (P < 0.05). The change in plasma 6-keto-PGF(1alpha) level in the AT III group was insignificant compared with the control group (P = 0.15). CONCLUSIONS: AT III prevented pulmonary infiltration of PMN and subsequent injury by the endothelial release of prostacyclin in CLP-induced sepsis.

Lipid peroxidation and antioxidant status in beta-thalassemia.

Autoxidation of globin chains and iron overload are the suggested mechanisms for the increased oxidative stress in beta-thalassemia. The aim of this study was to evaluate the extend of lipid peroxidation and antioxidant status of patients with beta-thalassemia and iron deficiency anemia (IDA) and compare the results with healthy subjects. Oxidant and antioxidant status of the children with beta-thalassemia major (n = 22) and iron deficiency anemia (n = 19) were studied. Healthy controls (n = 14) were age and sex matched. Fresh anticoagulated venous blood samples were obtained from all children. Conjugated diene (CD) and thiobarbituric acid-reactive (TBARS) substances were analyzed to indicate the oxidative parameters, whereas the erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx) were measured to show the antioxidant status of the children. Plasma TBARS and CD concentrations were elevated in beta-thalassemia compared to IDA. When compared to the controls, elevation in TBARS was significant. In the iron-deficiency group both TBARS and CD levels were decreased compared to the controls. SOD and GPx activities were increased in the beta-thalassemia group. SOD in beta-thalassemia was higher than both IDA and the controls and GPx activity was higher than the IDA group. In vivo lipid peroxidation was increased in children with beta-thalassemia major. This leads to a compensatory increase in antioxidant enzymes, whereas IDA does not lead to lipid peroxidation with a normal antioxidant enzyme activity.

Genotoxic, hematoxic, pathological, and biochemical effects of hexane on Swiss albino rats.

In the present study, the genotoxic, hematoxic effects, and their relation with pathological and biochemical parameters of hexane were investigated. Cytogenetic evaluation performed on the bone marrow indicated that chromosome aberrations increased at both hexane doses in relation to the negative controls. Decreased hematocrit, hemoglobin concentrations, and mean corpuscular volume were observed on the whole blood counts. Conjugated dienes (CD), glutathione (GSH), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and catalase (CAT) were increased. Histological examinations showed intracytoplasmic vacuolisation, nuclei with lower chromatin, and parenchymatous degenerations in the dose groups. In the bone marrow slides, depletion of the erythroid series were observed. In conclusion, hexane seems to be a genotoxic and hematoxic agent leading to degeneration and lipid peroxidation in exposed groups.

Effect of vitamin E supplementation on post-exercise plasma lipid peroxidation and blood antioxidant status in smokers: with special reference to haemoconcentration effect.

The oxidative effects were investigated of exhausting exercise in smokers, and the possible protective role of 400 mg day(-1) vitamin E (Vit E) supplementation over a period of 28 days. The subjects exercised to exhaustion including concentric-eccentric contractions following maximal cycling. The haematocrit and haemoglobin, leucocyte (WBC), plasma lactic acid (La) and malondialdehyde (MDA), erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx), serum Vit E and ceruloplasmin (CER) concentrations were measured pre and post exercise. Supplementation increased Vit E concentrations 28% and 31% in the controls and the smokers, respectively. Cigarette smoking and/or Vit E supplementation did not influence plasma lipid peroxidation or the antioxidant status at rest. Exercise caused significant haemoconcentration in all groups. When the post-exercise concentrations were adjusted for haemoconcentration, a significant elevation in La concentrations due to exercise was observed in all groups. Similarly, there were significant elevations in the adjusted WBC counts in all groups except the Vit E supplemented controls. The MDA concentrations on the other hand, when adjusted for haemoconcentration, did not exhibit any difference due to exercise. Exercise did not affect the GPx and CER activities either, while causing a SOD activity loss in all groups except the Vit E supplemented non-smokers. Serum Vit E concentrations diminished significantly in all groups after exercise. Post-exercise plasma MDA and blood antioxidant concentrations were not altered by smoking. The results would suggest that plasma volume changes should always be taken into account when assessing post-exercise plasma concentrations and that smoking and exercise do not have an additional collective effect on plasma lipid peroxidation and the dose of Vit E administered was insufficient to maintain the serum concentrations after exercise.

Prostaglandin synthetase inhibition reduces peritonitis-induced early liver oxidant stress.

This study was undertaken to determine whether or not the prostanoid metabolism contributes to peritonitis-induced early liver oxidant stress. Lipid peroxidation products, malondialdehyde (MDA) and conjugated dienes (CD), were used to monitor oxidant stress. The rats were given a 5-cc intraperitoneal (i.p.) injection of 25% rat feces suspension and then received either i.p. saline (peritonitis group, n = 11), vitamin E (n = 6), or diclofenac (n = 6). The liver and plasma MDA and CD levels were measured after 3 h. The plasma and liver MDA and CD levels were significantly higher in the peritonitis group than in the control (n = 9). Prostaglandin synthetase inhibitor (diclofenac) kept the liver and plasma MDA and CD at control levels. Antioxidant alpha tacopherol (vitamin E) was thus found not to be effective in reducing these increased MDA and CD levels. Peritonitis-induced early oxidant stress in the liver seems to be mediated by the oxidant-independent activation of the cyclooxygenase pathway.

Effects of vitamin E and cimetidine on peritonitis-induced lipid peroxidation.

To investigate the effects of acute fecal peritonitis on plasma and tissue lipid peroxidation and possible protective effects of vitamin E (Vit E) and cimetidine at 4 h in a rat peritonitis model, four groups were designated as: controls, peritonitis, Vit E and cimetidine. Plasma, liver, lung and kidney thiobarbituric acid reactive substances (TBARS) and conjugated diene (CD) levels were measured to monitor oxidative injury. The present fecal peritonitis model caused a significant elevation in liver TBARS; however, neither Vit E nor cimetidine was effective in preventing TBARS formation. Administration of Vit E and cimetidine caused significant decrements from the peritonitis value in liver and lung CD levels.

Antioxidant effect of alpha-tocopherol on fracture haematoma in rabbits.

In this study, the effect of free oxygen radicals on lipid peroxidation and the antioxidant role of alpha-tocopherol (vitamin E) in these reactions were investigated in haematoma fluid and venous blood samples in rabbits with femoral fracture. There were 21 male rabbits, divided into 3 groups. Conjugated dienes values (as optical density) were compared in venous blood of the rabbits in Group I taken preanaesthesia and after the onset of anaesthesia and the difference between these values proved to be insignificant (P > 0.05). A control group (Group 2) was given saline before fracture occurrence and the other group (Group 3) was injected with alpha-tocopherol 20 mg/kg intramuscularly. Venous blood samples and fracture haematoma fluids in both Group 2 and Group 3 were assayed biochemically. It was established that conjugated dienes values in fracture haematoma fluid in rabbits in the control group were higher than the values in the venous blood of the rabbits in the same group (P < 0.05). However, conjugated dienes values in the alpha-tocopherol injected group both in the haematoma fluid and in venous blood were reduced compared with those in the control group (P < 0.5). In view of the fact that ischaemia and reperfusion develop in fractured regions and that general body ischaemia develops following serious fractures of the extremities, we consider that prophylactic administration of antioxidants such as alpha-tocopherol may be beneficial in suppressing the destructive effects of free oxygen radicals in cells.