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Biomedical subjects

C M Caldarera

Publications and source records attributed to C M Caldarera.

At least 145 records · Page 8Linked to original sources
PubMed1965

Polyamines and nucleic acids during development of the chick embryo.

1. A higher concentration of polyamines (spermine, spermidine, putrescine and cadaverine) during development of the chick embryo was observed between the fifth and tenth day of incubation; the concentrations of nucleic acids showed a parallel increase. 2. When spermine (5mumoles) was injected into the yolk sac of embryos at the tenth day of incubation, a high amine-oxidase activity was noted and the spermine and spermidine concentrations were decreased; also, there was a remarkable decrease in RNA and DNA concentrations and a parallel increase in that of total free nucleotides. 3. On the other hand, when iproniazid (16mumoles) was injected there was an inhibition of amine-oxidase activity and a similar increase in the concentrations of spermine and spermidine and of nucleic acids, whereas that of total free nucleotides decreased. 4. Another group of embryos injected with spermine and iproniazid together showed a remarkable increase in spermine and spermidine concentrations and a parallel increase in those of RNA and DNA, and a decrease in that of total free nucleotides.

Journal Article↗
PubMedDate not supplied

Alpha-tocopherol pretreatment improves endothelium-dependent vasodilation in aortic strips of young and aging rats exposed to oxidative stress.

Acetylcholine-induced, endothelium-dependent relaxation of norepinephrine-precontracted aortic strips, was severely impaired after exposure to a hypoxanthine/xanthine oxidase reaction generating oxygen radicals. This effect was more evident in aortic strips of aging rats (24 months old) in comparison to young rats (3 months old). The addition of authentic .NO (1 microM) completely relaxed aortic strips exposed to oxidative stress both in young and aging rats. In vitro EPR measurements showed that the .NO signal was reduced by enzymatic O2.- generating reaction. The activity of a partial purified preparation of constitutive NO synthase from rat cerebellum was significantly decreased after exposure to exogenous oxygen radicals. Pretreatment of aortic strips with 100 microM alpha-tocopherol-phosphate, produced a significant improvement of acetylcholine-dependent relaxation in the aortic strips exposed to oxidative stress, particularly in the aged vessel. The content of malondialdehyde in aortic tissue did not change after oxidative stress or alpha-tocopherol pretreatment. Alpha-tocopherol was unable to recover the NO synthase activity depressed in vitro by hypoxanthine/xanthine oxidase reaction. This study confirms that an oxidative stress impairs the endothelium-mediated vasodilation. Alpha-tocopherol pretreatment protects the vessel against this damage. The mechanism of action of alpha-tocopherol is unknown, but seems unrelated to an antioxidant activity.

Acetylcholine↗
PubMedDate not supplied

Role of reactive oxygen species in cardiovascular aging.

Biochemical and structural changes occurring in the myocardium with aging are mainly resulting from the association of a general tissue atrophy with the hypertrophy of the remaining myocytes. Whilst hypertrophy seems to be a compensatory process to the loss of cardiomyocytes and to a mild systolic hypertensive condition that accompanies elderly people, atrophy should be the modification more closely related to aging 'per se.' In support to the free radical theory of aging, several signs of oxidative damage have been shown in the aged heart, such as lipofuscin accumulation, decreased phospholipid unsaturation index, greater formation of both hydrogen peroxide and 8-hydroxy-2'deoxyguanosine. As a compensatory reaction, the activities of the main oxygen-radical scavenger enzymes are stimulated in the mitochondria of aged rat heart. Endothelium-mediated vasoregulation is more susceptible to oxidative stress in aged with respect to young rats, suggesting that also the vasculature can be negatively influenced by the oxygen free radicals generated during aging. The possible primary role of oxygen free radicals in the development of myocardial atrophy is also discussed.

Acetylcholine↗
PubMedDate not supplied

Age-dependent production of mitochondrial hydrogen peroxide, lipid peroxides and fluorescent pigments in the rat heart.

Mitochondria were prepared from hearts of 3-, 14-, 18-, and 24-month-old male Wistar rats. Respiratory control ratio (RCR) values did not change with age in the glutamate or succinate-induced respiration except at 24 months in which RCR values significantly increased with both the substrates. Using still glutamate or succinate as substrates the production of H2O2 was measured in the presence of antimycin. A 70% and 25% increase in H2O2 formation was observed at 14 and 18 months of age, respectively, in comparison to the youngest group. Only in the presence of succinate was a 25% elevation in H2O2 found at 24 months of age. These observations parallel with the decrease of the ratio between tissue levels of reduced and oxidized glutathione that was observed at 14 and 18 months of age. The concentration of myocardial malondialdehyde, a secondary product of lipid peroxidation, remained the same at all ages measured, most probably because it is readily metabolized in vivo. On the contrary the myocardial level of lipofuscin, which is not degraded by the cell, progressively increased beginning from 18 months of age.

Aging↗
PubMedDate not supplied

Opioids stimulate sarcolemmal NAD(P)H-vanadate dehydrogenase activity.

The present study demonstrates that the bovine cardiac sarcolemma possesses an NAD(P)H dehydrogenase activity which is able to oxidize both NADH and NAD(P)H in the presence of vanadate as an electron acceptor. The NADH dehydrogenase activity was significantly higher than the NAD(P)H dehydrogenase activity and both of them were almost completely inhibited by superoxide dismutase and atebrin and markedly reduced by the addition of the protonophore 2,4-dinitrophenol. The incubation of the sarcolemma in the presence of 10(-10), 10(-9), 10(-8) M methionine-enkephalin, a prevalent delta-opioid receptor agonist, or dynorphin A (1-17), a prevalent kappa-receptor agonist, produced a dose-dependent increase in the NAD(P)H dehydrogenase activity, with 10(-10) and 10(-9) M dynorphin A (1-17) more effective than the corresponding doses of methionine-enkephalin. The preincubation of the sarcolemma in the presence of superoxide-dismutase, atebrin or 2,4-dinitrophenol strongly inhibited the opioid-stimulated dehydrogenase activity. The stimulatory action elicited by 10(-8) M methionine-enkephalin or dynorphin A (1-17) was completely antagonized by 10(-8) M naloxone or Mr 1452, respectively, whilst 10(-8) M naloxone exerted only a partially antagonistic action against the effect produced by 10(-8) M dynorphin A (1-17), significantly more accentuated than the action of 10(-8) M Mr 1452 versus the same dose of methionine-enkephalin.

Animals↗
PubMedDate not supplied

Effects of naloxone on the mechanical activity of isolated rat hearts perfused with morphine or opioid peptides.

In isolated rat hearts, the infusion for 10 min of 10(-10), 10(-8) or 10(-6) M (-)naloxone affected the cardiac function by markedly increasing the coronary pressure and by reducing both the heart rate and the developed tension. A lower dose of (-)naloxone (10(-11) M) or a dose of 10(-6) M (+)naloxone, did not modify the cardiac function. Morphine (10(-6) or 10(-5) M) and 10(-10), 10(-8) or 10(-6) M methionine-enkephalin or leucine-enkephalin, both significantly reduced the coronary pressure of the isolated rat hearts, during the first 4-6 min of perfusion, but the coronary pressure progressively increased above the control value in the last 4 min of perfusion. Each opioid also influenced the mechanical activity of the isolated rat heart, by significantly lowering both the heart rate and the developed tension. (-)Naloxone, at all the doses tested, was only able to antagonise the hypotensive effect induced by the opioids on the coronary pressure and was ineffective in counteracting the negative inotropic and chronotropic effects produced by each opioid. The perfusion in the presence of (+)naloxone (even at a dose of 10(-6) M) did not affect the opioid-induced changes on both the coronary pressure and the mechanical performance of the isolated heart.

Animals↗
PubMedDate not supplied

Inhibitory action of opioid peptides on ouabain-sensitive Na+-K+ and Ca2+-dependent ATPase activities in bovine cardiac sarcolemma.

The present study demonstrates that morphine (10(-6) and 10(-5) M), methionine-enkephalin or leucine-enkephalin (10(-10), 10(-8), and 10(-6) M) were able to inhibit significantly, in a dose-dependent manner, both the sarcolemmal Ca2+-dependent ATPase and the ouabain-sensitive Na+-K+ ATPase activities. The inhibitory action of these opioids on the two ATPases was not antagonized by preincubation with naloxone (10(-6) M). Naloxone alone (10(-8), 10(-6) and 10(-5) M) did not affect both the sarcolemmal Ca2+-dependent ATPase and the ouabain-sensitive Na+-K+ ATPase activities. Heat-denatured methionine-enkephalin (10(-6) M) or leucine-enkephalin (10(-6) M) also unaffected both the ATPases. The possibility is also discussed that opioid peptides may regulate myocardial contractility by modulating the movement of ions across the heart sarcolemma.

Animals↗
PubMedDate not supplied

Inhibitory effect of superoxide radicals on cardiac myofibrillar ATPase activity.

The superoxide radicals generated by the xanthine oxidase reaction reduced the myofibrillar Ca2+-ATPase activity. This negative effect was prevented by superoxide dismutase or by dithiothreitol, a protective thiol compound. Partial protection was achieved by catalase, while mannitol was ineffective. The myofibrillar Ca2+-ATPase exposed to O2-. radicals did not modify the affinity for Ca2+ while it showed a remarkable reduction of Vmax measured at the saturating level of Ca2+. The O2-. inhibited myofibrillar ATPase showed a higher value of Km for the cofactor associated to a reduced value of Vmax when studied in the presence of increasing concentration of ATP. Thus, circumstances that enhance the production of cardiac O2- radicals can be considered a negative metabolic event capable of depressing the myofibrillar Ca2+-ATPase activity.

Actomyosin↗
PubMedDate not supplied

Inhibitory effect of oxidized glutathione on heart ornithine decarboxylase activity.

Cardiac ODC was prepared from rats after the injection of isoproterenol and was partially purified by thiol-affinity chromatography. This enzymatic preparation incubated with GSSG was inactivated in a concentration dependent process. The inactivated enzyme could be reactivated by the addition of various reducing compounds, including GSH. Kinetic studies on GSSG-inactivated ODC revealed that the enzyme was inhibited by a partially-non competitive mechanism.

Animals↗
PubMedDate not supplied

Giovanni Moruzzi.

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Biochemistry↗