Previous studies from our laboratory have demonstrated the presence of complex alterations in the activities of antioxidant enzymes in various tissues of rats with streptozotocin (STZ)-induced diabetes. In the present investigation, it is shown that rats made diabetic with alloxan (ALX), an agent differing from STZ both chemically and in its mechanism of diabetogenesis, show virtually identical tissue antioxidant enzyme changes which, as is the case with STZ, are preventable by insulin treatment. The finding that the patterns of antioxidant enzyme alterations in chemically-induced diabetes are independent of the diabetogenic agent used and the presence of similar abnormalities in tissues of spontaneously diabetic (BB) Wistar rats (particularly when diabetic control is less than optimal) suggest that the changes observed are a characteristic feature of the uncontrolled diabetic state and that these may be responsible for (or predispose to) the development of secondary complications in clinical diabetes. Comparative studies involving red cells of diabetic rats and human diabetics revealed a number of common changes, namely an increase in glutathione reductase activity, a decreased susceptibility to oxidative glutathione depletion (which was related to the presence of hyperglycemia) and an increased production of malondialdehyde (an indirect index of lipid peroxidation) in response to in vitro challenge with hydrogen peroxide. In the diabetic patients, the extent of this increase in susceptibility of red cell lipids to oxidation paralleled the severity of diabetic complications. Our results suggest that increased (or uncontrolled) oxidative activity may play an important role in the pathogenesis of complications associated with the chronic diabetic state.
Propofol enhances red cell antioxidant capacity in swine and humansPurpose: To determine the effect of an anaesthetic with antioxidant potential, propofol, on red blood cell (RBC) antioxidant enzyme activities and RBC susceptibility to peroxidative challenge. Methods: Propofol was administered by intravenous bolus (2.5 mg.kg -~) and continuous infusion (36 and 72 ml'hr -J in nine swine; 216 ml-hr "-~ in two swine), to achieve serum concentrations between 5 and 30/Jg.ml -~ for two hours at each rate. Arterial blood sampling was at 0,10, 30, 60, and 120 min for each rate of infusion, for measurement of plasma propofol concentration, activities of plasma and RBC superoxide dismutase, glutathione peroxidase, gluthathione reductase, RBC catalase, and RBC malondialdehyde (MDA) formation in response to ex vivo oxidative challenge with t-butyl hydrogen peroxide (tBHP; I .SmM). Antioxidant mechanisms were determined by in vitro study of MDA formation, GSH depletion, and oxidation of haemoglobin to methaemogl0bin in human erythrocytes exposed to propofol 0-75/uM. The antioxidant potential of propofol was Compared with that of alpha-tocopherol utilising the reaction with 2,4,6-tripyridyl-s-triazine (TPTZ). Results: Propofol had no effect on plasma or RBC antioxidant enzyme activities. It inhibited RBC MDA production over the range of 0-20/ug.ml -~ (y = -I 8.683x + 85.431; R 2 = 0.8174). Effective propofol concentrations for 25% and 50% reductions in MDA levels were 7-12 and 12-20/ug.ml -t, respectively. Propofol has a similar effect on human erythrocytes in vitro (R 2 = 0.98). Conclusion" Propofol antagonises the effects of forced peroxidation of red cells at anaesthetic and sub-anaesthetic concentrations in swine. Its actions include scavenging of oxygen derived free radicals in a tocopherol-like manner.Objectif : D&erminer I'effet d'un agent anesth&ique poss~dant un potentiel antioxydant, le propofol, sur I'activit~ d'un enzyme antioxydant des globules rouges (GR) et sur la susceptibilit~ des GR ~ une provocation peroxydative. M&hodes : Le propofol a ~t~ administr~ en bolus intraveineux (2,5 mg'kg -I) et en infusions continues (36 et 72 ml.h -~ chez 9 porcs; 216 ml'h -~ chez 2 porcs) pour obtenir des concentrations s&iques entre 5 et 30/ug'mff durant deux heures ~. chaque vitesse d'infusion. Des pr~l~vements sanguins par voie art&ielle ont ~t~ r~alis& ~ 0, 10, 30, 60 et 120 min. pour chaque vitesse d'infusion; on a mesur~ la concent~tion de propofol, I'activit~ de la superoxyde dismutase du plasma et des GR, de la peroxydase du glutathion, de la r~ductase du glutathion, de la catalase du GR, ainsi que de la formation dans le GR de la malondialdehyde (MDA) en r~ponse ~ une provocation oxydative ex vivo avec le peroxyde d'hydrog~ne t-butylique (tBHP, 1,5 mM). Les m&anismes antioxydants ont &~ d~termin& par I'& tude in vitro de la formation de MDA, de la d~pl&ion de GSH ainsi que de I'oxydation de I'h~mogl0bine en meth& moglobine dans des GR humains expos& au propofol 0-75/~M. Le potentiel antioxydant du propofol a ~t~ comp...
The compounds Co(CF3SO3)2, Cu(CF3SO3)2, Co(CH3SO3)2, Cu(CH3SO3)2, Co(p-CH3C6H4SO3)2, and Cu(p-CH3C6H4SO3)2 have been prepared and infrared spectra, electronic spectra, and magnetic susceptibility studies are reported. Electronic spectral and magnetic studies have also been made on Cu(FSO3)2 and previously published data on Co(FSO3)2 are reexamined here. The studies indicate that in all salts the metal ions are hexacoordinated by oxygen atoms provided by anions acting as tridentate bridging ligands. The MO6 skeleton is significantly distorted from regular octahedral geometry for all salts with the possible exceptions of Co(FSO3)2, Co(p-CH3C6H4SO3)2, and Co(CH3SO3)2. Values of the spin–orbit coupling constants for the salts, as estimated from the magnetic studies, decrease with increasing anion basicity, suggesting a correlation between basicity and the degree of covalent character in the metal–anion bonds. In the case of the cobalt salts the interelectron repulsion parameter B also seems to decrease with increasing anion basicity.
Purpose: To compare low vs high dose propofol and isoflurane on red cell RBC antioxidant capacity in patients during aortocoronary bypass surgery (ACBP). Methods: Twenty-one patients, for ACBP, were anesthetized with sufentanil 0.5-10 ~ug.kg -I and isoflurane 0-2%; ISO = control; n=7), or sufentanil 0.3/./g'kg -t, propofol I-2.5 mg-kg -I bolus then 100/./g-kg-l-min -I before, and 50/Jg'kg-I'min -I during CPB (LO; n=7 ), or sufentanil 0.3/Jg'kg -I, propofol 2-2.5 mg-kg -t bolus then 200 /Jg.kg -I .min -I (HI; n=7 ). Venous blood was drawn pre-and post-induction, after 30 min CPB, 5, 10, and 30 min of reperfusion, and 120 min post-CPB to measure red cell antioxidant capacity (malondialdehyde (NDA) production in response to oxidative challenge with t-butyl hydrogen peroxide) and plasma propofol concentration. Pre-induction blood samples were analyzed for antioxidant effects of nitrates on red cells. The tBHP concentration response curves for RBC MDA in ISO, LO and HI were determined. Results: Preoperative nitrate therapy did not effect RBC MDA production. Perioperative RBC MDA production was similar in ISO and LO groups. Sustained intraoperative decrease in RBC IDA was seen with propofol 8.0 + 2.4 -I 1.8 ___ 4.5 g/g.ml "l in HI (P < 0.05-0.0001). MDA production vs log plasma propofol concentration was linear in HI dose. Conclusions: During CPB, RBC antioxidant capacity is enhanced and maintained with HI dose propofol. Propofol, at this dose, may prove useful in protecting against cardiopulmonary ischemia-reperfusion injury associated with ACBP.Objc~df : Comparer une faible dose (LO) vs une forte dose (HI) de propofol et d'isoflurane sur la capacit~ antioxydante des globules rouges (OR) lots d'un pontage aortocoronarien (PAC). M~thodc : Lots d'un PAC, 21 patients ont re~u une anesth&ie avec du sufentanil 0,5-I 0 Alg'l,,g -~ et de risoflurane 0-2 %; (ISO = t~moin, n = 7) ou du sufentanil 0,3 A/g-kg -I, un bolus de propofol I-2,5 mg.kg-lsuivi d'une perfusion de 100/.Ig'kg -I'min -I avant le PAC et de 50/~g'l,,g -I'min -I pendant le PAC (LO, n = 7 ), ou du sufentanil 0,3/Jg.kg -I , un bolus de propofol 2-2,5 mg'kg -I et une perfusion de 200 A/g-kg -I.min -I (HI, n = 7 ). Le sang veineux a ~t~ pr~lev~ avant et apr& I'induction, 30 rain apr~s le PAC, ~ 5, I 0 et 30 min pendant la repeffusion et 120 min apr~s la CEC afin de mesurer la capacit~ antioxydante des GR (production de diald~hyde malonique DAN en r~ponse ~ la provocation oxydante avec du peroxyde d'hydrog~ne t-butyl PHtB) et la concentration plasmatique de propofol. Les &hantillons de sang pr~lev6s avant I'induction ont &~ analys& pour v~dfler les effets antioxydants des nitrates sur les GR. Les courbes illustrant la r~action des GR au DAM chez les patients des groupes ISO, LO et Ht ont &~ d~termin~es. l~t~ts : La th~rapie pr~op6ratoire aux nitrates n'a pas chang~ la capacit?~ antioxydante des GR, donc la production de DAM a ~t~ semblable dans les groupes ISO et LO. Une baisse perop~ratoire de production de DAM atoutelois ~t~ observ& avec 8,0 ___ 2,4 -11,8 -+ 4.5...
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