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Biomedical subjects

L Cavallini

Publications and source records attributed to L Cavallini.

At least 55 records · Page 3Linked to original sources
PubMed1989

Effect of L-carnitine and L-aminocarnitine on calcium transport, motility, and enzyme release from ejaculated bovine spermatozoa.

Experiments were performed to further elucidate the role of gamma-amino-beta-hydroxybutyric acid trimethylbetaine (carnitine) on the metabolism and functions of spermatozoa. Addition of 20 mM L-carnitine to suspensions of ejaculated bovine spermatozoa resulted in an increase of cellular calcium transport, whereas 20 mM L-aminocarnitine (an inhibitor of carnitine palmitoyltransferase) caused an inhibition of this process. Both L-carnitine and L-aminocarnitine inhibited the progressive motility of spermatozoa, and the oxygen consumption as well as the release of the enzymes hyaluronidase and glutamate-oxaloacetate transaminase from spermatozoa. Labeled carnitine was rapidly taken up by spermatozoa by a process strongly dependent on temperature and extracellular concentration of carnitine. It is concluded that the effects produced by high concentrations of carnitine or aminocarnitine are mainly due to interactions of these compounds with the cellular membranes of spermatozoa.

Acyltransferases↗
PubMed1989

A morphometric study of the reversal of ACTH-induced hypertrophy of rat adrenocortical cells after cessation of treatment.

The effect of a prolonged (7-day) ACTH administration on rat zona fasciculata cells and its reversal after cessation of treatment was investigated by morphometry. ACTH treatment caused a notable cell hypertrophy, which was mainly due to the increase in the volume of the mitochondrial compartment and to smooth endoplasmic reticulum (SER) proliferation, and a conspicuous rise in the basal level of corticosterone. After cessation of ACTH administration, rat zona fasciculata cells underwent a time-dependent atrophy, so that after 5 days they resembled those of control animals, and the blood concentration of corticosterone reverted to the base-line value. The cell atrophy was provoked by the decrease in the volumes of the mitochondrial compartment and SER, and was associated with a striking time-dependent accumulation of dense bodies. Stereology demonstrated that during the first two days after ACTH withdrawal the decrease of SER prevailed over that of the mitochondrial compartment, while the reverse occurred during the remaining three days. The increase in the volume of dense-body compartment, though largely due to the accumulation of residual bodies, was mainly coupled with a rise in the volume of the microautophagic-vacuole compartment during the first two days after ACTH cessation and with an increase in that of the macroautophagic-vacuole compartment during the following three days. The hypothesis is advanced that both micro- and macroautophagy play a role in the reversal of ACTH-induced hypertrophy of rat zona fasciculata cells after cessation of treatment, the first process being mainly involved in the elimination of SER, and the second one in the degradation of mitochondria.

Adrenocorticotropic Hormone↗
PubMed1989

Stereological and functional investigations on isolated adrenocortical cells. I. Adrenocortical cells of normal adult rats.

The function and morphology of isolated rat adrenocortical cells were investigated. Capsular (zona glomerulosa) cells secreted aldosterone, progesterone and small amounts of corticosterone; inner (zonae fasciculata and reticularis) cells produced corticosterone and progesterone. ACTH (10(-8) M) exposure caused a striking rise in aldosterone and corticosterone secretion by capsular cells, and in corticosterone release by inner cell preparations; simultaneously, progesterone secretion was significantly reduced. Capsular and inner cells possessed an average volume of 500 and 1250 micron 3, and ultrastructural qualitative and quantitative (stereological) features closely resembling those of zona glomerulosa and zona fasciculata-reticularis cells in situ, respectively. ACTH exposure caused a notable lipid-droplet depletion in both types of isolated cells.

Adrenal Cortex↗
PubMed1989

Morphological and functional responses of rat Leydig cells to a prolonged treatment with human chorionic gonadotropins.

The morphological and functional responses of rat Leydig cells to a 3- and 6-day treatment with human chorionic gonadotropins (hCG) (10 IU/kg/day) were investigated by morphometric and radioimmunological techniques. hCG-administration induced a notable time-dependent enhancement in the steroidogenic capacity and growth of Leydig cells; this last was almost exclusively due to hypertrophy (and not to hyperplasia). The volume of mitochondrial and peroxisome compartments, as well as the surface area per cell of mitochondrial cristae and smooth endoplasmic reticulum (SER) were significantly increased after hCG treatment, and showed a highly significant positive linear correlation with both basal and stimulated testosterone production by isolated Leydig cells of the contralateral testis. Also the volume of nuclei and lipid-droplet compartment and the surface area per cell of Golgi apparatus displayed a notable hCG-induced rise, but they did not correlate with testosterone secretion. These findings suggest that, in addition to mitochondria and SER, in which the enzymes of steroid synthesis are located, peroxisomes are also specifically involved in the secretory activity of rat Leydig cells.

Animals↗
PubMed1989

Different buffers for hemodiafiltration: a controlled study.

Hemodiafiltration (HDF) is usually performed using a dialytic solution (D) containing acetate (A) or bicarbonate (B) and a replacement fluid (RF) containing lactate (L). To clarify the role of buffers in HDF, 11 patients underwent different study periods, each three months long: bicarbonate hemodialysis (BHD = Baseline period); HDF with (A) in D and (L) in RF (first period of HDF); HDF with (A) in D and (B) in RF (second HDF); HDF with (B) in D and (L) in RF (third HDF); HDF with (B) in D and (B) in RF (fourth HDF = BHDF). HDF achieved: 1) an increase in dialytic efficiency (kt/V, 1.28), reducing the time-session (197 min); 2) an improvement in acid-base status (pre-dialytic values in BHDF: pH 7.36; pCO2 39.8 mmHg; HCO3- 21.8 mM/L); 3) better "dry weight" gain (reached in 92.8% of HDF and in 81% of BHD sessions); 4) a significant decrease, in dialytic side-effects (mainly during the third and fourth periods). On the whole, BHDF (HDF done using only bicarbonate buffer) represents an easy and safe technique, leading to better cardiovascular stability than BHD and HDF without bicarbonate buffer.

Acetates↗
PubMed1988

Pathways of hydrogen peroxide generation in guinea pig cerebral cortex mitochondria.

The production of H2O2 by brain mitochondria was monitored employing a new technique based on the horseradish peroxidase dependent oxidation of acetylated ferrocytochrome c. It was shown that brain mitochondria release H2O2 by an intermediate autooxidation at the QH2-cytochrome c oxidoreductase level (induced by antimycin A and inhibited by myxothiazol). With both succinate and pyruvate plus malate this H2O2 release is inhibited at high substrate concentrations. With pyruvate plus malate a second source of H2O2 could be detected, apparently from autoxidation at the NADH dehydrogenase level. With alpha-glycerophosphate some H2O2 derives from autooxidation at the alpha-glycerophosphate dehydrogenase. The NADH dehydrogenase dependent, but not the QH2-cytochrome c oxidoreductase dependent H2O2 was significantly stimulated upon depletion of the mitochondrial glutathione.

Animals↗
PubMed1988

Effects of calcium chelators, divalent cations and sulfhydryl reagents on calcium uptake and motility of bovine spermatozoa.

Addition of 1 mM Ca/EGTA complex (1:1 ratio) to an incubation medium containing 1.5 mM Ca2+ produced a notable increase in the Ca2+ cycling in ejaculated bovine spermatozoa. Similar results were also obtained with the Ca/EDTA and Ca/EDTA complexes or with the heavy metal chelator DTPA (50 microM). Ba2+, Ni2+ or Co2+ added at 0.1 mM concentration abolished the stimulatory effect of the Ca/EGTA complex on Ca2+ cycling, whereas it did not affect the calcium movement in the absence of the calcium chelator complex. It is concluded that small amounts of these cations should be bound to the plasma membrane of bovine spermatozoa and inhibit the cellular calcium influx. 0.1 mM Cd2+ and NEM or 1 mM diamide produced a calcium efflux from the spermatozoa together with an inhibition of cellular motility and an increase in glutamate-oxaloacetate transaminase release. Conversely the impermeant sulfhydryl reagent mersalyl caused a net calcium efflux but did not alter the cellular motility nor the transaminase release. It is suggested that the permeant thiol reagents could decrease the spermatozoal mobility by impairing the mitochondrial ATP-synthesis.

Animals↗
PubMed1988

Evidence that long-term administration of a methionine-enkephalin analogue stimulates the growth and steroidogenic capacity of rat inner adrenocortical cells.

A prolonged infusion with D-ala2-met-enkephalinamide (DALA) caused a significant increase in both basal and ACTH-stimulated corticosterone secretion by dispersed inner adrenocortical cells of rats whose hypothalamo-hypophyseal axis was pharmacologically interrupted. This effect of DALA was associated with a notable hypertrophy of isolated cells. These findings suggest that enkephalins are involved in the stimulation of the growth and steroidogenic capacity of the cells of the inner layers of rat adrenal cortex.

Adrenal Cortex↗
PubMed1988

Modification of the xanthine-converting enzyme of perfused rat heart during ischemia and oxidative stress.

The reversible and irreversible conversion of xanthine dehydrogenase to xanthine oxidase during ischemia/reperfusion and oxidative stress induced by hydrogen peroxide or diamide and its relationship with glutathione and protein SH groups were studied. The direct spectrophotometric measurement of the various forms of the xanthine-converting enzyme indicates that, in the fresh rat heart or after normoxic perfusion, there always is a basal level of 80% xanthine dehydrogenase and 20% of xanthine oxidase (15% irreversible and 5% reversible) that could contribute to the background production of free radicals. There is no significant increase of irreversible xanthine oxidase during ischemia nor during reperfusion. After global ischemia the reversible oxidase shows almost no increase while, when ischemia is followed by reperfusion, there is a limited increase (less then 9%) of the reversible xanthine oxidase. In the latter conditions there is a decrease of glutathione and of SH groups of about 70% and 25%, respectively. Perfusion for 1 h with oxidizing agents like hydrogen peroxide (60 microM) or diamide (100 microM) determines a marked conversion of xanthine dehydrogenase to reversible xanthine oxidase of about 40% and 60%, respectively; this oxidase activity partially reconverts to the dehydrogenase after withdrawing the oxidizing agents from the perfusion medium. The level of irreversible xanthine oxidase remains unchanged in all the conditions tested. Both hydrogen peroxide and diamide induce a strong decrease in SH groups and depletion of glutathione. The xanthine dehydrogenase----xanthine oxidase conversion thus appears to be sensitive to the redox state of thiol groups.

Animals↗
PubMed1988

Effect of mevinolin on rat hepatocytes: a morphometric study.

A short-term (12 h) infusion with mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase, significantly lowered plasma cholesterol concentration in rats. After 7 days of continuous treatment hypocholesterolaemia disappeared, and this was coupled with a notable increase in the average volume of hepatocytes. Liver-cell hypertrophy was associated with a striking proliferation of the membranes of both rough and smooth endoplasmic reticulum, as well as with a tremendous increase in the number of peroxisomes. These structural changes are interpreted as the morphologic counterpart of the compensatory response of rat liver to the prolonged inhibitory effect of mevinolin on cholesterol synthesis.

Animals↗
PubMed1987

Decrease of serum malondialdehyde in patients treated with chlorpromazine.

Malondialdehyde determination in serum from schizophrenic patients before and after treatment with chlorpromazine showed that, after treatment, patients had significantly lower values than before. The antioxidant properties of chlorpromazine can be related to its effect on the level of serum lipid peroxides and possibly to its neuroleptic action.

Adult↗
PubMed1987

Prevention of lipid peroxidation by NAD(P)H in rat liver submitochondrial particles.

In rat liver submitochondrial particles both NADH and NADPH inhibit lipid peroxidation induced by cumene hydroperoxide. Concomitantly with the inhibition of lipid peroxidation, NADH and NADPH strongly stimulate the peroxidase activity of rat liver submitochondrial particles. Rotenone slightly prevents both the protective effect on malondialdehyde formation and peroxidase activity. The peroxidase activity of rat liver submitochondrial particles was attributed to the NAD(P)H-mediated reduction of mitochondrial cytochrome P-450 which can act upon hydroperoxides, by decomposing them to alcohols.

Alcohols↗
PubMed1985

Inhibition of rat liver hydroxymethylglutaryl-CoA reductase by sulfhydryl reagents, coenzyme A esters and synthetic compounds.

The activity of the microsomal 3-hydroxy-3-methylglutaryl-coenzyme A reductase was assayed with a procedure based on the extraction of the product mevalonolactone in a benzene phase. Diamide is an uncompetitive inhibitor of the reaction, while coenzyme A disulfide and tetraethylthiouram disulfide act as non-competitive inhibitors. Diamide inhibition cooperatively increases with the inhibitor concentration. HMG produces a decrease in enzyme activity that combines with that of coenzyme A disulfide. Both CoASH and coenzyme A esters strongly inhibit the reductase activity. Three new synthetic compounds with either thio-ether or thio-ester groups also show inhibitory effect on the enzyme activity.

Acyl Coenzyme A↗
PubMed1985

Inhibitory action of quercetin on xanthine oxidase and xanthine dehydrogenase activity.

Quercetin is an equally good inhibitor of xanthine oxidase (type O, oxygen-reducing enzyme) and xanthine dehydrogenase (type D, NAD+-reducing enzyme) activity of a preparation of the xanthine-oxidizing enzyme partially purified from rat liver. The inhibition seems competitive with the oxidase form and non-competitive (mixed-type) with the dehydrogenase form of the enzyme. These inhibitory properties should be referred to the flavonoid structure of quercetin rather than to its antioxidant power. The antioxidant properties of quercetin and its inhibitory effect on the xanthine-oxidizing enzyme are discussed with reference to hyperuricemic and ischemic states.

Animals↗
PubMed1985

Inhibition of lipid peroxidation by alpha-tocopherolquinone and alpha-tocopherolhydroquinone.

The antioxidant effect of alpha-tocopherolquinone and alpha-tocopherolhydroquinone was studied in liposomes and rat liver submitochondrial particles. Both alpha-tocopherolquinone and alpha-tocopherolhydroquinone inhibit lipid peroxidation induced by ascorbate/Fe2+ in liposomes and by cumene hydroperoxide in submitochondrial particles. Alpha-tocopherolhydroquinone is much more effective than alpha-tocopherolquinone in inhibiting lipid peroxidation. Submitochondrial particles, depleted of ubiquinones and reincorporated with alpha-tocopherolquinone, are protected from lipid peroxidation only in the presence of succinate. Alpha-tocopherolquinone cannot replace endogenous ubiquinones in the respiratory chain function, nevertheless it can be reduced by the mitochondrial respiratory chain substrates, presumably through the reduced ubiquinones.

Animals↗
PubMed1984

Comparison of cumene hydroperoxide- and NADPH/Fe3+/ADP-induced lipid peroxidation in heart and liver submitochondrial particles. Mechanisms of protection by succinate.

The NADPH/Fe3+ /ADP system stimulates lipid peroxidation both in rat liver and bovine heart submitochondrial particles, while cumene hydroperoxide is active only in rat liver submitochondrial particles. The lack of a peroxidizing effect of cumene hydroperoxide in heart submitochondrial particles was related to the absence of cytochrome P-450. When ubiquinones are extracted from rat liver and bovine heart submitochondrial particles, succinate can still partially protect the cumene hydroperoxide-induced lipid peroxidation but not the peroxidation induced by NADPH/Fe3+ /ADP. The protective effect of succinate in lipid peroxidation was referred either to the reduction of ubiquinones that can act as antioxidants in the NADPH/Fe3+ /ADP system, or to the reduction of cytochrome P-450 that acts as a peroxidase in the cumene hydroperoxide system.

Adenosine Diphosphate↗