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Red blood cells from alcoholics with and without liver cirrhosis and control subjects were examined for the susceptibility to lipid peroxidation. Red blood cells of patients with liver cirrhosis were found to be less sensitive to hydrogen peroxideinduced peroxidation measured by a new, reliable and sensitive method: the release of pentane during red blood cell lipid peroxidation. Changes of sensitivity to lipid peroxidation correlated with the severity of the liver malfunction, but not with abnormalities of the lipid composition of red cell membranes which are apparent in patients with liver disease. In alcoholics without liver cirrhosis, only minor changes in the susceptibility of red cells to peroxidation were observed.

Red blood cells from 31 healthy donors were examined for the cholesterol content, the fatty acid composition, and the susceptibility to lipid peroxidation induced by either hydrogen peroxide or phenylhydrazine. Lipid peroxidation was monitored by the release of pentane and ethane. In addition, plasma fatty acids were measured in order to find out, whether plasma and red cell fatty acids were correlated. In experiments with hydrogen peroxide, a significant positive correlation was found between the proportion of arachidonic acid (C 20:4n - 6; r = 0.57, p less than 0.01) and docosahexaenoic acid (C 22:6n - 3; r = +0.71, p less than 0.01), and the release of pentane and ethane, respectively. A significant negative correlation was found between the membrane cholesterol content and the pentane release (r -0.44, p less than 0.05). In experiments performed with phenylhydrazine, red cell membrane lipid composition did not influence the susceptibility of red cells to lipid peroxidation. A close correlation was found between plasma and red cell fatty acids (palmitic acid, r = +0.46, p less than 0.01; linoleic acid, r = +0.41, p less than 0.05; arachidonic acid, r = +0.59, p less than 0.01; docosahexaenoic acid, r = +0.67, p less than 0.01). The results demonstrated that the degree of peroxide-induced oxidation of erythrocyte lipids depends on the content of polyunsaturated fatty acids in the membrane, which on the other hand, is determined by plasma fatty acids. It is suggested that dietary variations may influence the susceptibility of red cells to lipid peroxidation.

The blood from 19 patients having bone marrow transplantation was examined for the essential antioxidants alpha-tocopherol and beta-carotene as well as lipid hydroperoxides before, at and after bone marrow transplantation (BMT). Conditioning therapy, preceding BMT in order to achieve marrow ablation and immunosuppression, consists of high-dose chemotherapy which is mostly combined with total body irradiation (TBI). In order to see a possible difference between patients with and without additional TBI, we divided the patients up into two groups; patients receiving TBI (RT+) and patients without TBI (RT-). All patients required total parenteral nutrition beginning one week prior to BMT. After conditioning therapy plasma levels of absolute and lipid-standardized alpha-tocopherol and beta-carotene decreased in both groups, presumably as a result of an enhanced breakdown of these antioxidants. The loss of these lipid-soluble antioxidants has to be considered as a possible cause for early post-transplant toxicity. Lipid hydroperoxides increase significantly in the group of patients with additional TBI, whereas the other group, receiving no additional TBI, showed no significant change. We suggest high-dose supplementation of essential antioxidants for patients undergoing BMT.

Erythrocytes might be expected to be highly susceptible to peroxidation. Their membranes are rich in polyunsaturated fatty acids; they are continuously exposed to high concentrations of oxygen; and they contain a powerful transition metal catalyst. In fact, autoxidation is held in check in vivo by extremely efficient protective antioxidant mechanisms. These involve cellular enzymes such as superoxide dismutase and glutathione peroxidase, as well as vitamin E; but they mainly reflect effective structural compartmentalisation. This review surveys mechanisms which lead to red cell lipid autoxidation and the role of haemoglobin in these processes. The influence of haemoglobinopathies, of lipid composition and of abnormalities in antioxidant mechanisms induced by exogenous oxidant stress is also considered.

Die bisher veroffentlichten optischen Verfahren zur Bestimmung von Kohlenoxydhamoglobin im Blut und deren Fehler werden erortert.

In der vorliegenden Arbeit wird ein neues, einfaches Verfahren zur Isolierung der Glutathionreductase aus Blutzellen beschrieben. Die Reinigung des Enzyms erfolgte durch Ammoniumsulfatfraktionierung und saulenchromatographische Verfahren.

Es wird eine Methode zur quantitativen Bestimmung von α-Aminosauren durch manometrische Messung der bei der Reaktion von Aminosauren mit dem Natriumsalz von p-Toluolsulfonchloramid freigesetzten Kohlensaure beschrieben. Die Messung erfolgt in der Warburg-Apparatur. Die optimalen Reaktionsbedingungen werden untersucht und Spezifitat, Empfindlichkeit und Genauigkeit des Verfahrens gepruft.

A group of 46 patients with melphalan-resistant multiple myeloma was treated according to the M-2 protocol with melphalan, prednisolone, BCNU, cyclophosphamide, and vincristine. According to the Salmon and Durie classification, four patients had stage II A; 36, stage III A; and six, stage III B disease. Treatment resulted in five patients (11%) entering remission, while 21 (46%) had stable and 20 (43%) had progressive disease. The median survival for all patients was 12.5 months, patients in remission surviving longer (median 46 months) than those with stable disease (median 15.4 months) or progressive disease (median 6.9 months). Compared with other treatment regimens used in melphalan-resistant myeloma, the remission rate is low but the median survival exceeds that reported by most other authors.

Vinylchloride (VC) was identified by gas chromatography-mass spectrometry as a decomposition product of 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU). VC was observed in blood and exhaled air from patients after administration of BCNU. Production of VC is evident even after incubation of blood from normal donors with BCNU.

Human red blood cells and male Sprague-Dawley rats were treated in vitro and in vivo , respectively, with phenylhydrazine in order to determine whether the release of volatile hydrocarbons can serve as a suitable index for phenylhydrazine-induced red blood cell peroxidation. Lipid peroxidation following phenylhydrazine administration ( in vitro experiments: dosage calculated at 0.5–50mM; in vivo experiments: intraperitoneal injection of 2.8 mg/100g body wt) was monitored by the release of ethane and pentane measured by gas chromatography. Further hydrocarbons such as ethylene, propane, n -butane, iso -butane and iso -butene were monitored to form a basis of comparison. In vitro haemolysis was also determined during the course of incubation. Red blood cell suspensions yielded more than 15-fold concentrations of propane and more than 2-fold concentrations of iso -butane compared to pentane and ethane yields. Haemoglobin solutions also produced propane and iso -butane in the presence of phenylhydrazine, whereas pentane and ethane were not detectable. Time-course studies revealed that ethane and pentane reached maximum in vitro levels after red blood cell suspensions had been incubated for 2 hr whereas the maximum degree of haemolysis (approximately 60%) was attained between 60 and 90 min following the beginning of phenylhydrazine treatment. The dosage did not affect the final degree of haemolysis. Rats treated with phenylhydrazine exhaled greater concentrations of ethane (6-fold increase) and pentane (2-fold increase) compared to control animals. Exhaled propane showed a 30-fold increase in concentration following drug treatment. Our results suggest that the release of pentane and ethane may be useful in assessing red blood cell lipid peroxidation in the presence of phenylhydrazine in vitro and in vivo .

Publisher Summary This chapter describes the preparation and stability of glucose-6-phosphate dehydrogenase (G6P-DH). G6P-DH was first isolated from erythrocytes and by fermenting yeast. It has been demonstrated in practically all animal tissues and in micro-organisms. Blood cells, adipose tissue, and the lactating mammary gland that are especially rich sources of the enzyme. Some human and animal tumors contain a high concentration of this enzyme. The optimum pH of the G6P-DH reaction is 8.3 for the enzyme from yeast or blood cells. It is found that between pH 7.4 and 8.6 there is little change in the enzyme activity. The measurements are made at pH 7.5 because this is nearest to physiological conditions and allows comparison to be made with other enzyme activities which are usually measured at this pH. The accuracy of the determination of activity in liver tissue can be increased if the hemoglobin content of the supernatant is estimated, and on the basis of this estimation, the additional G6P-DH is calculated. This value is subtracted from the total G6P-DH activity of the liver homogenate.