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Biomedical subjects

L Manzo

Publications and source records attributed to L Manzo.

At least 91 records · Page 5Linked to original sources
PubMed1986

Thallium-induced testicular toxicity in the rat.

Reproductive tract functions were studied in adult male Wistar rats given 10 ppm thallium as thallium sulfate in the drinking water. After 60 days of treatment, spermatozoa isolated from the cauda epididymides and vas deferens showed reduced motility and immature germ cells were found in the tubular lumen. Histological examination of testes in thallium-treated animals revealed disarrangement of the tubular epithelium and ultrastructural changes in the Sertoli cells with cytoplasmic vacuolation and distension of the smooth endoplasmic reticulum. The activity of testicular beta-glucuronidase was significantly reduced whereas acid phosphatase and sorbitol dehydrogenase activities were unchanged. Plasma testosterone levels were within normal limits. No abnormalities in testicular morphology and biochemistry were seen in animals sacrificed at the end of the first month of thallium exposure. These findings indicate that the male reproductive system is a susceptible target site to toxic effects of thallium under chronic exposure. They also suggest a major involvement of Sertoli cells in the mechanism underlying thallium-induced testicular damage.

Acid Phosphatase↗
PubMed1985

Depression by morphine of the excitability of intrinsic inhibitory neurons in the guinea-pig colon.

The mechanical responses to morphine were examined in isolated preparations of longitudinal and circular muscle of the guinea-pig colon. In the longitudinal coat, morphine induced a relaxation which was prevented by naloxone, hyoscine and tetrodotoxin. Conversely, in the circular coat morphine caused a contraction which was antagonized by naloxone, mimicked by tetrodotoxin and left unaltered by hyoscine, chlorpheniramine and methysergide. In both muscular layers, morphine depressed (and tetrodotoxin abolished) the non-adrenergic relaxation induced by field stimulation. The action of morphine in the two preparations can thus be explained in terms of inhibition of the tonic excitatory cholinergic or inhibitory non-adrenergic neural control prevailing in the longitudinal and circular muscle respectively.

Animals↗
PubMed1985

Behavioral and eegraphic changes induced by dopaminergic antidepressants in rabbits.

Nomifensine, Bupropion and Amineptine, "second generation" antidepressants with dopaminergic effects, were studied in the rabbit with special regard to their action on somatic and autonomic behavior, and cerebral electrical activity. All three drugs induced an "alarm" reaction and typical dopaminergic behavioral responses including sniffing, jumping and chewing. Mydriasis was also observed especially at high dose levels. EEG showed an arousal pattern for each of these drugs. A marked increase in the hippocampal spiking resulted from the i.v. administration of 15 mg/kg of Bupropion.

Animals↗
PubMed1984

Erythromycin estolate impairs the mitochondrial and microsomal calcium homeostasis: correlation with hepatotoxicity.

The effects of erythromycin estolate, a well known hepatotoxic macrolide antibiotic, on isolated rat hepatocyte viability and on subcellular Ca2+ transport have been investigated. Erythromycin estolate (0.5 mM), but not erythromycin base and erythromycin ethylsuccinate, induced 100% cell death after 60 min incubation, and caused maximal inhibition of mitochondrial and microsomal Ca2+ sequestration activities at 0.1 mM concentration. Sodium lauryl sulphate, which is the surfactant moiety of the erythromycin estolate molecule, caused effects similar to those exhibited by erythromycin estolate. Disorders of the intracellular calcium homeostasis seem to play a role in the lauryl sulphate-mediated hepatotoxic action of erythromycin estolate.

Animals↗
PubMed1984

Intestinal absorption and excretion of thallium (201Tl) in the rat.

The gastrointestinal transport of 201Tl-labelled monovalent thallium has been studied in normal and rats with cannulated bile ducts using an in vivo ligated loop technique. A marked difference in the Tl absorptive capacity among the various sections of the gut was observed. 201Tl was taken up more quickly from the colon than from any other segment and the uptake from the ileum and jejunum was higher than from the stomach. In addition, considerable amounts of the intravenously administered thallium were excreted into the intestinal lumen. The biliary excretion was very low compared with the direct transfer of 201Tl across the gastrointestinal wall that occurred against a tissue-to-plasma concentration gradient. In the rat, the large intestine seems to be the major area for the enteral reabsorption and recycling of thallium (I) ions.

Animals↗
PubMed1983

Purine receptors in the guinea-pig internal anal sphincter.

1 In the isolated internal anal sphincter of the guinea-pig, adenosine 5'-triphosphate (ATP) and adenosine induced a concentration-dependent and tetrodotoxin-insensitive relaxation. 2 Pretreatment with theophylline (25-50 microM) had no significant effect on the concentration-response curves obtained with either purine compound. 3 Reactive blue 2 (25-100 microM) shifted the curve to ATP to the right in a dose-dependent fashion leaving that to adenosine unaltered. The antagonism appeared to be non-competitive. 4 Neither reactive blue 2 nor purine receptor occupation by ATP or adenosine altered the electrically-induced non-adrenergic, non-cholinergic inhibitory response. 5 The actions of ATP and adenosine in the guinea-pig internal anal sphincter appear to be mediated by separate receptors. These receptors are not involved in the nerve-mediated relaxation.

Adenosine↗
PubMed1983

Dilazep: an inhibitor of adenosine uptake with intrinsic calcium antagonistic properties.

Concentrations of dilazep which were ineffective in altering the muscular tone of the guinea-pig taenia caeci (0.03, 0.3 microM) or the phasic mechanical activity of the rabbit proximal ileum (0.03 microM) markedly potentiated the inhibitory action of adenosine on both these parameters. Dilazep, 0.3 microM or greater, dose-dependently inhibited the mechanical activity of the proximal ileum. This inhibitory action was probably mediated by more than one mechanism, as shown by the fact that theophylline (50, 100 microM) antagonized the effect at lower dilazep concentrations (up to 3 microM) leaving essentially unchanged the response to higher concentrations (6, 10 microM). Similarly, the responses to low doses of dilazep were reduced after desensitization of the organ to adenosine, whilst the responses to higher doses were unaffected by this procedure. In a Ca2+-free, high-K+ medium, dilazep (1-10 microM) caused a parallel shift to the right of the Ca2+-induced contractions of the guinea-pig taenia caeci. Adenosine showed only slight Ca2+-antagonistic properties within the mM range of concentrations. These findings suggest that, at the higher concentration tested, dilazep exhibits Ca2+-antagonistic properties unrelated to its adenosine-mediated mode of action.

Adenosine↗
PubMed1983

Biliary and gastrointestinal excretion of chromium after administration of Cr-III and Cr-VI in rats.

Rats treated intravenously with 51Cr-labelled sodium chromate, 0.1 or 100 microgram Cr/rat, excreted more 51Cr into bile in a 2-hr period than did the animals given equal amounts of chromium in the trivalent state. Distinct patterns of hepatic intracellular distribution of the radiotracer were also observed. In the Cr-VI rats over 50% of the liver chromium was present in the supernatant fraction whereas in the Cr-III rats almost all the liver radioactivity was localized in the cell organelles. Fractionation of bile on Sephadex G-75 demonstrated binding of chromium to low-molecular weight substances. It is suggested that complexes of chromium with low-molecular weight components of liver cytosol are involved in the passage of this element from the liver to bile. A low cytosolic content of diffusable Cr-complexes associated with the incorporation of a large fraction of liver chromium in cell organelles may be a factor contributing to the low rates of 51Cr biliary excretion in the animals given Cr-III. 24 hr after the injection of 51Cr to bile duct-ligated rats appreciable levels of radiotracer were found in the gastrointestinal tract. The animals given Cr-VI exhibited significantly higher values of chromium content in the gut than those treated with Cr-III.

Animals↗
PubMed1983

EEG profile of the anticonvulsant action of viloxazine in the rabbit.

The intravenous administration of the bicyclic antidepressant viloxazine, 0.5-2 mg/kg in rabbits, caused changes in the EEG profile with increased synchronous activity and shorter duration of the hippocampal afterdischarge following electrical stimulation. In animals exhibiting spontaneous epileptiform discharges, the injection of 1-2 mg/kg viloxazine was associated with disappearance of the paroxysmal EEG pattern that was substituted by a synchronous low frequency activity. This study also provided evidence of non-interactive effects of viloxazine (1-2 mg/kg i.v.) and alcohol (0.6 g/kg i.v.) on the EEG of normal rabbits.

Animals↗
PubMed1982

Organ/tissue disposition of thallium in pregnant rats.

The placental transfer of thallium was studied in rats treated with a toxic dose of thallium sulphate (10 mg Tl/kg b.wt. p.o.), as well as in animals injected intraperitoneally with 201Tl-labelled thallium in amounts as low as 2 micrograms Tl/rat. Rapid uptake and retention of thallium in both maternal and fetal organs were observed. The administration of potassium ferrihexacyanoferrate II (100 mg/kg b.wt. twice daily by gavage) to rats acutely intoxicated with thallium on day 17 of pregnancy resulted in significant decrease of thallium concentrations in various maternal tissues including brain, in the placenta as well as in the fetal liver and brain. Potassium ferrihexacyanoferrate II also reduced the mortality of pregnant animals in the 72-h interval after the intoxication.

Animals↗
PubMed1982

Placental transfer and retention of 201Ti-thallium in the rat.

Placental transfer of thallium was evidenced in rats treated with a single intraperitoneal dose of 2 micrograms 201T1-labelled thallium/rat on the 13th day of pregnancy. Both maternal and fetal organs showed remarkable thallium retention, approx. 10% of the dose being unexcreted 8 days after injection. The highest thallium accumulation was found in maternal muscle and brain tissues. Fetal brain exhibits higher thallium uptake and faster decay rate of thallium levels than maternal brain. It is suggested that the reduced activity of the mechanisms regulating ion movements and composition of nervous tissue and the immaturity of the blood-brain barrier play a role in the peculiar pattern of thallium kinetics in the developing rat brain.

Animals↗
PubMed1982

Effects of naloxone on ethanol and acetaldehyde-induced electroencephalographic changes in rabbits.

Rabbits treated with a single IV dose of ethanol, 0.6 g/kg, exhibited rapid EEG synchronization and behavioral changes that were reversed and, in part, prevented by the opiate antagonist, naloxone, 40 micrograms/kg. The continuous intracerebroventricular infusion of acetaldehyde, 10 or 120 micrograms/min. caused biphasic changes with EEG activation and severe bradycardia followed by overt synchrony during the post-infusion period. The results of the present study provide further evidence for the ability of naloxone to counteract some acute effects of ethanol. Moreover, they do not support a role of acetaldehyde itself as mediator of EEG changes associated with mild alcohol intoxication.

Acetaldehyde↗
PubMed1981

Biliary excretion of vanadium in rats.

The biliary excretion of vanadium was studied in bile duct cannulated rats at various times after the iv administration of a single dose of 48V-labelled pentavalent vanadium. The tissue disposition, hepatic intracellular distribution and binding of 48V to plasma, bile and liver components were also investigated. During the first 6 hours after the injection of V, 0.9 to 30 microgram/kg, less than 2 per cent of the dose was excreted into the bile and up to 20 per cent of vanadium was eliminated in urine. The bile flow was markedly decreased in rats cannulated 24 hours after the injection of V, 30 microgram/kg, while higher doses produced signs of severe toxicity immediately after the administration. Evidence was also obtained that a concentration gradient triggers the passage of vanadium from plasma to the liver, where only a fractional amount becomes available from canalicular excretion, due to the extensive binding of the metal to organelles and other tissue ligands.

Animals↗
PubMed1980

Salivary levels of thallium in acute human poisoning.

Thallium intoxication in a 28-year-old woman was characterized by neurological and gastrointestinal symptoms and alopecia. Treatment was started 4 days after poisoning and consisted of forced diuresis and administration of Prussian Blue at four daily doses of 5 g by duodenal tube for 20 days. Thallium was measured by atomic absorption spectrophotometry in urine, faeces and saliva. Considerable amounts of thallium were detected in saliva, salivary concentrations being up to 15 times higher than urinary ones. Evidence was also obtained that only a little fraction of the ingested dose was excreted by the intestine during the hospital course in spite of Prussian Blue administration.

Acute Disease↗
PubMed1980

Effects of phenobarbitone on the distribution, metabolism and biliary excretion of erythromycin in rats.

The administration of phenobarbitone to the rat (8 mg/100 g BW) once daily for 3 days significantly decreased the serum and tissue levels of erythromycin administered intraperitoneally (5 mg/100 g BW). Furthermore, phenobarbitone stimulated the hepatic microsomal N-demethylation of erythromycin and increased the biliary concentration and the biliary excretion rate of the unmetabolized antibiotic. These effects were accompanied by augmented liver mass and bile flow. The possibility is discussed that erythromycin concentrates in the bile through a specialized hepatic drug transport system, activated by phenobarbitone.

Animals↗
PubMed1979

Aminopyrine: metabolism and effects in the rat after administration of inhibitors of hepatic monooxygenases.

The administration to the rat of the inhibitors of microsomal mixed function oxidase, SKF 525A and Oxine-5-sulphonic acid (OSA) caused a significant decrease of the hepatic aminopyrine N-demethylase activity, as well as an increase in the plasma levels and antipyretic activity of orally administered aminopyrine. The plasma concentrations of the aminopyrine metabolite 4-aminoantipyrine were reduced in SKF 525-A treated animals while they were slightly increased in those pretreated with OSA. These findings suggest that the in vivo changes of aminopyrine disposition and activity brought about by SKF 525-A were the result of an inhibited hepatic drug metabolism, while the effects produced by OSA were due to a more rapid intestinal absorption of aminopyrine.

Aminopyrine↗