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PubMed1999

Copper-adenine catalyst for O(2) production from H(2)O(2).

In solutions of CuCl2 and adenine copper can be bound to adenine. Two Cu(adenine)(2) complexes [Cu(C(5)H(5)N(5))(2)]2+/Cu(C(5)H(4)N(5))(2)] are in equilibrium with free adenine. Copper-adenine complexes present a catalytic activity (e.g., H(2)O(2) disproportionation into O(2) and water) but depending on complex concentration H(2)O(2) also strongly oxidizes the adenine within the complexes. Raman spectroscopy quantifies copper-adenine complex formation and H(2)O(2) consumption; polarography quantifies O(2) production. As for C(40) catalase, optimal catalytic capacities depend on physiological conditions, such as pH and temperature. The comparative analysis of kinetic parameters shows that the affinity for H(2)O(2) of Cu(adenine)(2) is 37-fold lower than that of C(40) catalase and that the molar activity for O(2) production is 200-fold weaker for Cu(adenine)(2) than for the enzyme. In the 10(-6)-10(-3) M range, the strong decrease of activity with raising complex concentration is explained by aggregation or stacking, which protects Cu(adenine)(2) entities from H(2)O(2) oxidation, but also decreases O(2) production.

Adenine↗

PubMed2000

A possible role of the Na(+)/K(+)-ATPase for O(2) production from H(2)O(2).

We are attempting to supply a new insight on interaction between Na(+)/K(+)-ATPase and H(2)O(2). We demonstrate that in vitro the Na(+)/K(+)-ATPase, a non heme-protein, is able to disproportionate H(2)O(2) catalatically into dioxygen and water, as well as C(40) catalase. By polarography, we quantify O(2) production and by Raman spectroscopy H(2)O(2) consumption. A comparative analysis of kinetics parameters relative to O(2) production shows that for Na(+)/K(+)-ATPase the affinity of the catalytic site able to transform H(2)O(2) into O(2) is twice weaker than that for C(40) catalase. It also shows that the molar activity for O(2) production is 300-fold weaker for ATPase than for catalase. Inhibitors, pH and GSH studies highlight the differences between the heme- and nonheme-proteins. Indeed, for C(40), NaN(3) is strongly inhibiting, but much less for ATPase. The pH range for the catalatic activity of ATPase is wide (6.5 to 8.5), while it is not for C(40) catalase (optimum at pH 8). The Na(+)/K(+)-ATPase catalatic activity is reduced in presence of glutathione, while it is not the case with C(40) catalase.

Animals↗

PubMed2001

Do denervated peripheral nerve trunks become ischemic? The impact of chronic denervation on vasa nervorum.

The long-term relationship between the peripheral nerve trunk and its vascular supply, the vasa nervorum, has not been considered in the context of denervation and regeneration. While the microvessels of peripheral nerve are not thought to influence Wallerian degeneration itself, in this work we explored how vasa nervorum respond to denervation of the nerve trunk. Our hypotheses were that the presence of axons had a significant impact on the vasa nervorum and that the absence of reinnervation might eventually lead to an unfavorable ischemic regenerative microenvironment. We studied rat sciatic nerve trunks for up to 6 months following transection and either prevented regeneration or allowed it to proceed. Vasa nervorum were studied in several ways: (i) measurements of local endoneurial blood flow using microelectrode hydrogen clearance polarography; (ii) measurements of erythrocyte flux (flow) in the extrinsic nerve plexus using laser Doppler flowmetry; (iii) India ink perfusion of microvessels in unfixed nerve; (iv) mRNA expression of vascular endothelial growth factor (VEGF) using reverse transcription polymerase chain reaction. Early after injury, there were rises in endoneurial and extrinsic flow, microvessel numbers, and VEGF mRNA expression. Angiogenesis was apparently confined to the epineurial and perineurial compartments. Later, however, there were substantial declines in flow observed in long-term (6-month) denervated sciatic nerve trunks associated with declines in the caliber of new microvessels. Reinnervated sciatic nerves had restored endoneurial blood flow. The findings confirm important relationships between axon presence and local blood flow. Angiogenesis is a feature of the injured peripheral nerve, but long term denervated nerve trunks have declines of flow despite retaining new microvessels.

Animals↗

PubMed1999

Solution-Membrane Equilibrium at Metal-Deposited Cation-Exchange Membranes: Chronopotentiometric Characterization of Metal-Modified Membranes.

Copper- and lead-deposited interpolymer cationic membranes have been prepared by electroless plating by an ion-exchange method and characterized by chronopotentiometry and cyclic voltammetry. The parameters such as transition time (tau), Itau1/2, the potential drop (E0) across these membranes immediately after the application of constant current (I), and the height of the potential jump (DeltaE) across the membrane at tau have been measured by chronopotentiometry and compared with those of plain membranes. The approximate percentage of metal coverage and the number of ionic sites masked by the deposited metal in terms of NaCl concentration have been estimated from the differences in Itau1/2 values of plain and metal-deposited membranes. The quantity of metal deposited in a unit area of the membrane surface was measured by differential pulse polarography. The oxidation and reduction peak potentials corresponding to Cu(0)/Cu(II) and Pb(0)/Pb(II) couples were identified by cyclic voltammetry at pH 2.8 and 4.5 of 0.2 M CH3COONa-H2SO4. Copyright 1999 Academic Press.

Journal Article↗

PubMed2002

Effect of coenzyme Q10 supplementation on mitochondrial function after myocardial ischemia reperfusion.

BACKGROUND: Coenzyme Q10 (CoQ10) protects myocardium from ischemia-reperfusion (IR) injury as evidenced by improved recovery of mechanical function, ATP, and phosphocreatine during reperfusion. This protection may result from CoQ10's bioenergetic effects on the mitochondria, from its antioxidant properties, or both. The purpose of this study was to elucidate the effects of CoQ10 supplementation on mitochondrial function during myocardial ischemia-reperfusion using an isolated mitochondrial preparation. METHODS: Isolated hearts (n = 6/group) from rats pretreated with liposomal CoQ10 (10 mg/kg iv, CoQ10), vehicle (liposomal only, Vehicle), or saline (Saline) 30 min before the experiments were subjected to 15 min of equilibration (EQ), 25 min of ischemia (I), and 40 min of reperfusion (RP). Left ventricular-developed pressure (DP) was measured. Mitochondria were isolated at end-equilibration (end-EQ), at end-ischemia (end-I), and at end-reperfusion (end-RP). Mitochondrial respiratory function (State 2, 3, and 4, respiratory control index (RCI, ratio of State 3 to 4), and ADP:O ratio) was measured by polarography using NADH (alpha-ketoglutarate, alpha-KG)- or FADH (succinate, SA)-dependent substrates. RESULTS: CoQ10 improved recovery of DP at end-RP (67 +/- 11% in CoQ10 vs 47 +/- 5% in Vehicle and 50 +/- 11% in Saline, P < 0.05 vs Vehicle and Saline). CoQ10 did not change preischemic mitochondrial function. IR decreased State 3 and RCI in all groups using either substrate. CoQ10 had no effect in the mitochondrial oxidation of alpha-KG at end-I. CoQ10 improved State 3 at end-I when SA was used (167 +/- 21 in CoQ10 vs 120 +/- 10 in Saline and 111 +/- 10 ng-atoms O/min/mg protein in Vehicle, P < 0.05). Using alpha-KG as a substrate, CoQ10 improved RCI at end-RP (4.2 +/- 0.2 in CoQ10 vs 3.2 +/- 0.2 in Saline and 3.0 +/- 0.3 in Vehicle, P < 0.05). Using SA, CoQ10 improved State 3 (181 +/- 10 in CoQ10 vs 142 +/- 9 in Saline and 140 +/- 12 ng-atoms O/min/mg protein in Vehicle, P < 0.05) and RCI (2.21 +/- 0.06 in CoQ10 vs 1.85 +/- 0.11 in Saline and 1.72 +/- 0.08 in Vehicle, P < 0.05) at end-RP. CONCLUSIONS: The cardioprotective effects of CoQ10 can be attributed to the preservation of mitochondrial function during reperfusion as evidenced by improved FADH-dependent oxidation.

Animals↗

PubMed2002

Ischemic preconditioning improves mitochondrial tolerance to experimental calcium overload.

BACKGROUND: Ca(2+) overload leads to mitochondrial uncoupling, decreased ATP synthesis, and myocardial dysfunction. Pharmacologically opening of mitochondrial K(ATP) channels decreases mitochondrial Ca(2+) uptake, improving mitochondrial function during Ca(2+) overload. Ischemic preconditioning (IPC), by activating mitochondrial K(ATP) channels, may attenuate mitochondrial Ca(2+) overload and improve mitochondrial function during reperfusion. The purpose of these experiments was to study the effect of IPC (1) on mitochondrial function and (2) on mitochondrial tolerance to experimental Ca(2+) overload. METHODS: Rat hearts (n = 6/group) were subjected to (a) 30 min of equilibration, 25 min of ischemia, and 30 min of reperfusion (Control) or (b) two 5-min episodes of ischemic preconditioning, 25 min of ischemia, and 30 min of reperfusion (IPC). Developed pressure (DP) was measured. Heart mitochondria were isolated at end-Equilibration (end-EQ) and at end-Reperfusion (end-RP). Mitochondrial respiratory function (state 2, oxygen consumption with substrate only; state 3, oxygen consumption stimulated by ADP; state 4, oxygen consumption after cessation of ADP phosphorylation; respiratory control index (RCI, state 3/state 4); rate of oxidative phosphorylation (ADP/Deltat), and ADP:O ratio) was measured with polarography using alpha-ketoglutarate as a substrate in the presence of different Ca(2+) concentrations (0 to 5 x 10(-7) M) to simulate Ca(2+) overload. RESULTS: IPC improved DP at end-RP. IPC did not improve preischemic mitochondrial respiratory function or preischemic mitochondrial response to Ca(2+) loading. IPC improved state 3, ADP/Deltat, and RCI during RP. Low Ca(2+) levels (0.5 and 1 x 10(-7) M) stimulated mitochondrial function in both groups predominantly in IPC. The Control group showed evidence of mitochondrial uncoupling at lower Ca(2+) concentrations (1 x 10(-7) M). IPC preserved state 3 at high Ca(2+) concentrations. CONCLUSIONS: The cardioprotective effect of IPC results, in part, from preserving mitochondrial function during reperfusion and increasing mitochondrial tolerance to Ca(2+) loading at end-RP. Activation of mitochondrial K(ATP) channels by IPC and their improvement in Ca(2+) homeostasis during RP may be the mechanism underlying this protection.

Adenosine Diphosphate↗

PubMed1995

Neuroprotective effects of carvedilol in diabetic rats: prevention of defective peripheral nerve perfusion and conduction velocity.

The effects of carvedilol (10 mg kg-1 day-1), a peripheral vasodilator and oxygen free radical scavenger, on nerve conduction and blood flow were examined in streptozotocin-diabetic rats. Rats were treated from induction of diabetes for 1 month in a preventive experiment; effects of treatment in non-diabetic rats were also examined. Diabetes caused a 20.0% (P < 0.001) reduction in sciatic motor conduction and a 14.7% (P < 0.001) deficit in saphenous sensory conduction. Diabetic rats given carvedilol treatment had motor and sensory conduction velocities which did not differ significantly from those of non-diabetic controls, but were greater than for untreated diabetes (P < 0.001). Carvedilol treatment did not significantly alter nerve conduction in non-diabetic rats. The nutritive (capillary) component of sciatic endoneurial blood flow, measured by microelectrode polarography and hydrogen clearance, was 45.8% (P < 0.001) reduced by diabetes. This was completely corrected (P < 0.001) by carvedilol treatment in diabetic rats, flow being in the upper half of the non-diabetic range. In non-diabetic rats, carvedilol caused a 30.6% (P < 0.05) elevation in blood flow. Hydrogen clearance data also revealed a shift away from non-nutritive (arterio-venous anastomotic) towards nutritive flow in treated diabetic rats (P < 0.05). We conclude that the data support a neurovascular hypothesis of diabetic neuropathy. Carvedilol, via vasodilator and anti-oxidant actions, prevents the nutritive blood flow changes that lead to nerve dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1982

Changes in brain blood flow associated with deltamethrin-induced choreoathetosis in the rat.

Deltamethrin is a pyrethroid insecticide which produces reversible motor symptoms in mammals involving facial movements, progressive incoordination, and choreoathetosis. These symptoms were found to be preceded and accompanied by increases in blood flow in the caudate nucleus and cerebral cortex of conscious rats. Blood flow, measured by the hydrogen polarography method, showed a 2.8-3.8 fold increase in the caudate nucleus and a 1.9-2.6 increase in the cortex after intraperitoneal deltamethrin. The increase in caudate blood flow provided an early and sensitive indicator of the development of motor symptoms, and preceded development of EEG spike discharges. A different pattern of motor symptoms consisting largely of tremor with no choreoathetosis was produced for comparison using another pyrethroid, cismethrin. This, whilst producing a similar increase in cortical flow, did not produce the disproportionate increase in caudate flow characteristic of deltamethrin. Although the actions of deltamethrin were shown not to be restricted to the extrapyramidal system, the selectivity of the blood flow increases, and the nature of the symptoms produced show deltamethrin to be a useful tool for the production of experimental extrapyramidal motor hyperactivity.

Animals↗

PubMed1994

Alpha-domain of human metallothionein IA can bind to metals in transgenic tobacco plants.

With a view to exploring its use as a metal-binding factor in transgenic plants we prepared the alpha-domain of metallothionein by reconstitution of rabbit apometallothionein and proteolysis of MT-1 and MT-2 with subtilisin. The isolated alpha-domains were characterised by UV and CD spectroscopy Double-Stranded. DNA encoding the alpha-domain (106 bp) of the human MT-IA was constructed from chemically synthesized oligomers by repair synthesis and enzymatic ligation, cloned into pUC19 and sequenced. A expression construct containing the cloned alpha-domain was introduced into tobacco cells on a disarmed Agrobacterium tumefaciens Ti-plasmid. Transformed tobacco cells were selected and regenerated on medium containing cadmium and kanamycin. The growth of roots and shoots of transformants was unaffected by up to 100 microM cadmium, whereas control plants showed severe inhibition of root and shoot growth, and chlorosis of leaves on medium containing only 10 microM cadmium. Southern hybridization confirmed the presence of the transgene in the transformed plant tissues. The concentration of human alpha-domain peptides in transgenic tobacco leaves was determined by the Cd/hemoglobin saturation assay and polarography using the rabbit alpha-domain as standard. The results indicate that the alpha-domain, one of two domains in MT molecules, is not only stable in vitro, but is also expressed efficiently and functions independently in transgenic plant cells.

Agrobacterium tumefaciens↗

PubMed1995

Oxidized cellulose causes focal neuropathy, possibly by a diffusible chemical mechanism.

We observed incidentally that rat sciatic nerve in contact with oxidized cellulose (OC), an absorbable hemostatic agent, underwent focal fiber degeneration, and we undertook studies to determine the mechanism of its production. Topically applied OC generated acute nerve damage within the adjacent nerve fascicle of rat sciatic nerve in a dose-dependent fashion (r = 0.99, P < 0.01, threshold amount: 9.9 mg). IN single teased fibers, the predominant type of myelinated fiber damage was axonal degeneration. The subperineurial blood flow of the rat sciatic nerve was serially measured by microelectrode hydrogen polarography, and the reduction at 90 min after application of OC was not greater than that of controls. A thin polyethylene membrane interposed between OC and the sciatic nerve almost completely prevented the nerve damage. These data suggest that the chief mechanism of nerve damage by OC was neither compression nor ischemia, but was a diffusible chemical mechanism. Care should be taken to avoid direct OC application around peripheral nerves.

Animals↗

PubMed1994

The potential contribution of endothelin-1 to neurovascular abnormalities in streptozotocin-diabetic rats.

Abnormal vascular endothelium function may contribute to the reduced nerve perfusion implicated in the aetiology of neuropathy in diabetes mellitus. The aim was to test the hypothesis that a powerful vasoconstrictor, endothelin-1, could be involved in nerve dysfunction in streptozotocin-diabetic rats. After 6 weeks of untreated diabetes, rats were implanted with osmotic minipumps which continuously delivered the endothelin-1 antagonist, BQ-123, to the circulation via a jugular vein cannula. Sciatic motor conduction velocity, monitored serially, was increased after 4 days, treatment (p = 0.028), and reached asymptote by 9-11 days (p = 0.0001), when the degree of amelioration was approximately 60% of the initial diabetic deficit. Treatment of non-diabetic rats for 13 days with BQ-123 had no significant effect on motor conduction velocity. Sensory saphenous nerve conduction velocity was measured acutely after 20 days, BQ-123 treatment. The amelioration of a sensory deficit was approximately 80% (p < 0.001); the resultant conduction velocity value was not significantly different from that of a non-diabetic control group. After 20 days, treatment, sciatic nutritive endoneurial blood flow was measured by microelectrode polarography and hydrogen clearance. A 48% deficit with untreated diabetes (p < 0.001) was 64% ameliorated by BQ-123 treatment (p < 0.001). In non-diabetic rats, BQ-123 treatment had no effect on blood flow. We conclude that endothelin-1 does not seem to be involved in the control of nerve blood flow in non-diabetic rats; however, it makes a major contribution to the perfusion deficit in experimental diabetes. This has deleterious consequences for nerve conduction, and it is possible that endothelin-1 receptor blockade may have therapeutic potential in diabetic patients.

Analysis of Variance↗

PubMed1995

Effects of natural free radical scavengers on peripheral nerve and neurovascular function in diabetic rats.

Increased generation of reactive oxygen species, coupled with impaired endogenous scavenging mechanisms, plays a prominent role in the aetiology of neurovascular abnormalities in experimental diabetes mellitus. We examined the efficacy of the natural anti-oxidants vitamins C, E and beta-carotene in preventing nerve conduction and nutritive blood flow deficits in streptozotocin-diabetic rats. One month of diabetes caused a 19.1% reduction in sciatic motor conduction velocity (p < 0.001). This was approximately prevented 80-90% by high-dose (1000 mg.kg-1.day-1) vitamin E and beta-carotene treatments (p < 0.001). Vitamin C had lesser effects; the maximum protection found for motor conduction velocity was 36% using a dose of 150 mg.kg-1.day-1 (p < 0.001). High dose (500 mg.kg-1.day-1 (p < 0.001). High dose (500 mg.kg-1.day-1) vitamin C had a lesser effect on conduction than intermediate doses. Joint vitamin C and lower dose (500 mg.kg-1.day-1) vitamin E treatment had a predominantly additive preventive effect against nerve dysfunction. Resistance to hypoxic conduction failure for sciatic nerve in vitro was markedly increased by diabetes and this remained relatively unaffected by treatment. Sciatic nutritive endoneurial blood flow, measured using microelectrode polarography and hydrogen clearance, was reduced 46.1% by 1 month of diabetes (p < 0.001). This was prevented to the extent of 87%, 36% and 98% by vitamins E, C and beta-carotene, respectively (p < 0.01). These data emphasize the role of oxidative stress in the development of early neurovascular changes in experimental diabetes and show that naturally available scavengers have a neuroprotective action.

Action Potentials↗

PubMed1994

Aldose reductase inhibition, nerve perfusion, oxygenation and function in streptozotocin-diabetic rats: dose-response considerations and independence from a myo-inositol mechanism.

We examined the effects of aldose reductase inhibition on nerve biochemistry and function, blood flow and endoneurial oxygenation in experimental diabetes mellitus. After 1 month untreated diabetes in rats, treatment with the novel sulphonylnitromethane aldose reductase inhibitor, ZENECA ZD5522, prevented a progressive increase in sciatic nerve resistance to hypoxic conduction failure (p < 0.05). Motor conduction velocity deficits after 4 months untreated diabetes were rapidly returned to normal within 12 days (p < 0.0001) by ZD5522 treatment. Following 2-months untreated diabetes, examination of 1 month ZD5522 treatment dose-response relationships for correction of nerve sorbitol and fructose accumulations and reduction in myo-inositol concentration, sciatic motor and saphenous sensory conduction velocity and sciatic blood flow by laser-Doppler flowmetry revealed poor agreement between nerve function and biochemical indices. In addition, polyol accumulation differed between sciatic and saphenous nerves, the latter showing ten-fold lower sorbitol concentrations. Laser-Doppler blood flow was 60% decreased by untreated diabetes (p < 0.001) and there was a strong correlation between ZD5522-mediated increases in blood flow and conduction velocity (p < 0.0001). Measurement of nutritive endoneurial blood flow by microelectrode polarography and hydrogen clearance showed 44% and 45% deficits for 1 and 2 months untreated diabetes (p < 0.001) that were prevented by ponalrestat and ZD5522 treatments, respectively. In contrast, 2 months myo-inositol treatment from diabetes induction did not prevent reduction in blood flow or sciatic motor conduction velocity. A 37% reduction in endoneurial oxygen tension after 2 months diabetes (p < 0.001) was completely prevented by ZD5522 treatment (p < 0.001). The data show that a very high degree of polyol pathway blockade is necessary to correct nerve functional deficits and that aldose reductase inhibitors have a neurovascular action that does not depend on restoration of nerve myo-inositol.

Acetanilides↗

PubMed1991

Relationship between cochlear blood flow and perilymphatic oxygen tension.

To clarify the characteristics of the blood circulation in the cochlea, we correlated cochlear blood flow and perilymphatic oxygen tension at various blood pressures. Cochlear blood flow was measured in guinea pigs by laser Doppler flowmetry, and perilymphatic oxygen tension by polarography. Blood pressure changes were induced by angiotensin II injection, trimetaphan camsylate injection and blood withdrawal. Cochlear blood flow generally paralleled systemic blood pressure, indicating a close correlation. In contrast, perilymphatic oxygen tension was slower to increase and decrease. However, when systemic blood pressure was lowered more gradually, perilymphatic oxygen tension did not show the same lag. These findings indicate that perilymphatic oxygen tension parallels systemic blood pressure when changes induced are slower and in a physiological range.

Angiotensin II↗

PubMed1991

Pharmacokinetics of fotemustine and BCNU in plasma, liver and tumor tissue of rats bearing two lines of Walker 256 carcinoma.

The plasma and tissue pharmacokinetics of fotemustine (diethyl-1-[3-(2-chlorethyl)-3-nitrosoureido]-ethylphosphonate+ ++) and BCNU (1,3-bis-[2-chlorethyl]-1-nitrosourea) were investigated in healthy control rats and in animals bearing either the nitrosourea-sensitive line A (W256/A) or the nitrosourea-resistant line B (W256/B) of Walker 256 carcinoma. The antitumor activities of these nitrosoureas were similar following i.v. doses ranging from 10 to 40 mg/kg. For both drugs, the survival of tumor-bearing rats was lower in the W256/B than in the sensitive W256/A line. Some sex differences were observed, female rats being more responsive than males to both drugs. Nitrosourea concentrations were assayed in plasma and tissues by differential pulse polarography so as to assess whether the pharmacokinetics could explain the differences in antitumor activity. The antineoplastic effects of fotemustine seemed to be influenced by its pharmacokinetics. The plasma AUC of the intact nitrosourea was higher in females than in males. Fotemustine was cleared 2-5 times more slowly than BCNU from tumor tissue, and its clearance was higher in W256/B- than in W256/A-bearing rats. This suggests that the antitumor activity in the responsive line might partly be due to longer exposure of the growing tumor to the drug. The distribution volume of both nitrosoureas in plasma was higher in tumor-bearing animals than in healthy controls, indicating that the tumor tissue probably constitutes an additional distribution space.

Animals↗

PubMed1986

History of blood gas analysis. IV. Leland Clark's oxygen electrode.

The electrochemical reduction of oxygen was discovered by Heinrich Danneel and Walter Nernst in 1897. Polarography using dropping mercury was discovered accidentally by Jaroslav Heyrovsky in Prague in 1922. This method produced the first measured oxygen tension values in plasma and blood in the 1940s. Brink, Davies, and Bronk implanted platinum electrodes in tissue to study oxygen supply, or availability, from about 1940, but these bare electrodes became poisoned when immersed in blood. Leland Clark sealed a platinum cathode in glass and covered it first with cellophane; he then tested silastic and polyethylene membranes. In 1954 Clark conceived and constructed the first membrane-covered oxygen electrode having both the anode and cathode behind a nonconductive polyethylene membrane. The limited permeability of polyethylene to oxygen reduced depletion of oxygen from the sample, making possible quantitative measurements of oxygen tension in blood, solutions, or gases. This invention led to the introduction of modern blood gas apparatus.

Animals↗

PubMed1980

An electrochemical analysis of changes in properties of DNA caused by ionizing and ultraviolet radiations.

Electrooxidation and electroreduction of gamma- and u.v.-irradiated DNA were studied by means of differential pulse voltammetry at the graphite electrode and differential pulse polarography at the dropping mercury electrode. Two separated voltammetric oxidation peaks G and A were used for monitoring conformational changes in guanine . cytosoine (GC) and adenine . thyminde (AT) pairs respectively in irradiated double-stranded (ds) DNA. Pulse-polarographic reduction peak III was used for detection of denatured DNA in the irradiated samples of ds DNA. It was found that the heights of peaks G and A of ds DNA did not change with the radiation dose after relatively low doses of gamma- and u.v.-radiations (up to ca. 40 krads and 1 X 10(4) Jm-2, respectively, when no single-stranded (ss) DNA was detected in the irradiated DNA samples. After higher doses of radiation the occurrence of ss DNA or ss segments in the irradiated samples of ds DNA was accompanied by an increase of peaks G and A; however, peak A grew more rapidly with the increasing dose than peak G. It was concluded that the results obtained support the assumption, according to which regions of ds DNA rich in AT pairs are more susceptible to denaturation caused by gamma- and u.v.-radiations.

Cobalt Radioisotopes↗

PubMed1976

Structure and function of cardiac mitochondria in exhausted guinea pigs.

The ultrastructure and functional capacity of mitochondria from hearts of exhausted guinea pigs were compared to those from rested animals. Electron micrographs of heart ventricles were examined for ultrastructural alterations, and functional capacity was studied by oxygen polarography. General swelling of mitochondria from exhausted animals was indicated by a 41% reduction in mitochondrial surface/volume ratio and a 22% increase in volume density of mitochondria from exercised animals when compared to those from controls. The yield of isolated mitochondria from exhausted guinea pigs was similar to that for control animals. In the presence of all substrates tested the rate of oxygen consumption was lower in the exhausted animals than in the controls. The ADP/O ratios and respiratory control indices for pyruvate, succinate and ascorbate were not systematically affected by exercise. With glutamate as substrate respiratory control was reduced in exercised guinea pigs. These experiments suggest that the structure of myocardial mitochondria from exhausted animals is sufficient to maintain normal ADP/O ratios but is not adequate to maintain normal rates of respiration.

Animals↗