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Biomedical subjects

A Marzi

Publications and source records attributed to A Marzi.

13 recordsLinked to original sources
PubMed1989

Effect in vivo of endogenous sexual hormones upon the liver mitochondrial function compared in male and female diabetic rats.

Chronic diabetes induced by the injection of streptozotocin in male and female albino adult rats provoked significant alteration of liver mitochondrial function 30 or 35 days after administration of the drug. Thus, we obtained mean values of respiratory control (RC) and state 3 (S3) with 3-hydroxybutyrate as substrate 40 or 50% lower than those of non-diabetic animals. With other substrates (malate-glutamate, succinate) the decrease of RC and S3 in the diabetic animals was 20% or 30% of the normal mean values. The osmotic damped oscillations of mitochondria were measured as another parameter of the organella function. It was assayed with valinomycin as K+ ionophore and succinate as substrate. In diabetic rats of both sexes we found a significant increase of the mean damping factor of these oscillatory variations compared with normal values. The above-mentioned results indicate a lesser elasticity and an impaired K+ transport of mitochondria across the inner membrane in diabetic animals. Both reported parameters, respiration and oscillatory variations of liver mitochondria, were measured in normal non-diabetic rats and in the groups of diabetic rats referred to as follows: 1) intact (male and female), 2) gonadectomized (male and female), 3) oophorectomized with restitution of 17 beta-estradiol. Ovariectomized diabetic rats showed a significant increase in the values of the RC and S3 of liver mitochondria compared with intact female diabetic animals. The withdrawal of the ovarian hormone in female diabetic rats significantly decreased the values of the damping factors of the oscillatory mechanism and they were similar to the normal. The restitution of 17 beta-estradiol to oophorectomized diabetic rats resulted in a decrease of liver mitochondrial respiration. The damping factor of liver mitochondria of the oophorectomized diabetic rats treated with the estrogen showed values significantly higher than those of female diabetic animals without the hormone and similar to the values of the intact diabetic female rats. Castration of male rats did not produce any effect upon the liver mitochondrial RC and S3 or upon the mean damping factor of the oscillatory variation either. Then the castration of male diabetic rats did not modify the mitochondrial function. In contrast, the oophorectomy of diabetic animals produced amelioration of mitochondrial respiration and oscillatory behavior. The conclusion is drawn that in female rats the circulating 17 beta-estradiol produced a pernicious effect upon liver mitochondrial function in the experimental diabetic state.

Animals↗
PubMed1982

Chicken resistance to dimethylnitrosamine acute effects on the liver: a comparative study with other species.

Dimethylnitrosamine (DMN)-induced liver damage, as measured by the increase in plasma isocitrate dehydrogenase as well as by histologic assessment of necrosis, was marked after DMN ip administration (70 mg/kg) in males of all noninbred species tested (BALB/c mouse, Sprague-Dawley rat, Syrian golden hamster, general purpose guinea pig) but not in the noninbred White Leghorn chicken. At 1 and 3 hours after DMN injection, liver DMN levels were not lower in the chicken as compared to levels in the other species. Furthermore, in all species except the chicken, significant decreases were found at 3 hours as compared to 1 hour after DMN administration. DMN metabolism to CO2 and to formaldehyde, as well as covalent binding of DMN-reactive metabolites to either proteins or nucleic acid, was measured with the use of liver slices, microsomes, and/or 9,000 X g supernatants. Results indicated that chicken liver had a very low capacity for metabolism and activation (29-3,166 times lower than comparable data in mice or hamsters).

Animals↗
PubMed1981

Effects of cysteine and cystamine on the carbon tetrachloride induced decrease in arachidonic acid content of rat liver microsomal phospholipids.

Cystamine and cysteine inhibited the carbon tetrachloride (CCl4) prooxidant effect on rat liver microsomal preparations, at concentrations ranging from 0.001 mM to 1 mM. Cysteine exhibited a biphasic effect being an inhibitor of the prooxidant action at concentrations below 0.1 mM and acting as an enhancer at 1 mM. Cystamine but not cysteine pretreatment of the rats prevented the CCl4 induced decrease in the arachidonic acid content of liver microsomal phospholipids. However, both cystamine and cysteine led to decreases in arachidonic acid similar to that produced by CCl4 but they do not have deleterious effects on the liver. These results cast doubt on the role of lipid peroxidation in the liver cell injury by CCl4.

Animals↗
PubMed1981

Enhancement of the dimethylnitrosamine acute effects in rat liver by prior treatment with triton WR-1339.

Prior administration of Triton WR-1339 (tyloxapol, an anionic surfactant) to noninbred Sprague-Dawley male rats significantly enhanced the intensity of the necrogenic effect of dimethylnitrosamine (DMN) on the liver. This phenomenon was established by determination of NADP+-linked isocitrate dehydrogenase activity in the plasma and by histologic procedures. This enhancing effect was not due to an increase in the levels of DMN that reached the liver, because the content of DMN in the livers of Triton WR-1339-treated or untreated animals at 1 or 3 hours was not significantly different. Triton WR-1339 administration had no effect on DMN liver metabolism to formaldehyde or CO2; in addition, the covalent binding of DMN metabolites to nucleic acids or proteins was not modified by pretreatment with Triton WR-1339. However, in vitro, high concentrations (1 mg/ml) of Triton WR-1339 decreased the intensity of these parameters. This effect disappeared when the concentration was lowered to 0.4 mg/ml. Results are compatible with the hypothesis that the potentiating effects of Triton WR-1339 on liver damage caused by DMN and other hepatotoxins were due to a modification of the response of liver cells to injury.

Animals↗
PubMed1980

Studies on the prevention of CCl4 induced liver necrosis by agents having effects on cell membrane.

Nupercaine, promazine and benadryl partially prevented liver injury produced by CCl4 given orally, 24 hours after administration, in contrast to cetyl trimethyl ammonium bromide and anthisan which did not show any effect. Only benadryl and anthisan were able to partially prevent liver damage at 24 hours caused by ip administration of CCl4. None of these compounds decreased CCl4 content in liver at 1; 3 or 6 hours after oral CCl4 administration. Results suggest that benadryl could prevent liver necrosis, changing the cell response to injury by CCl4.

Administration, Oral↗
PubMed1980

Promethazine administration to rats and CCl4 induced lipid peroxidation of liver microsomal lipids.

Promethazine inhibited CCl4 stimulated microsomal lipid peroxidation in vitro at concentrations ranging from 10(-3) to 10(-8)M. CCl4 administered to rats at a dose of 1 ml/kg decreased the arachidonic acid content of microsomal lipids after 6 hours of intoxication. Prior promethazine treatment, at dosage regimes that preclude CCl4 induced liver necrosis at 24 hours, did not significantly prevent the CCl4 induced decrease in arachidonic acid content. Moreover, promethazine itself produced a similar decrease but in complete absence of liver damage. Results suggest that either lipid peroxidation is not relevant to liver injury or that the arachidonic acid decrease in microsomal lipids is not evidence for lipid peroxidation occurrence or that promethazine effects are not related to inhibition of lipid peroxidation.

Animals↗
PubMed1980

Pyrazole prevention of CC14-induced ultrastructural changes in rat liver.

Carbon tetrachloride (CC14) administration to rats leads to an early dilatation, vesiculation and disorganization of the liver endoplasmic reticulum (ER). This hepatotoxin also causes detachment of ribosomes from ER membranes, dilatation of the Golgi cisternae and occasionally dilatation of the perinuclear membrane. Prior treatment of the rats with pyrazole completely prevents CC14- induced ultrastructural alterations observed in liver at 3 h. This drug is known to decrease the intensity of the irreversible binding of CC14 reactive metabolites to cellular constituents without modifying the intensity of the CC14- induced lipid peroxidation, either in vitro or in vivo, as measured by the diene conjugation procedure or by decreases inthe arachidonic acid content of microsomal phospholipids. Results suggest that interaction of reactive metabolites rather than lipid peroxidation mediates deleterious effects of CCl4 on the liver ER.

Animals↗
PubMed1976

Alpha-Glutamyl-beta-naphthylamide hydrolase of rabbit small intestine. Localization in the brush border and separation from other brush border peptidases.

About 70% of the total mucosal enzymatic activity hydrolyzing beta-L-glutamyl-beta-naphthylamide in the rabbit small intestine is present in the brush border; the specific activity in this subcellular fraction is 7 times higher than that of the homogenate. Similar results are obtained for L-leucyl beta-naphthylamide hydrolase. The enzyme activity is efficiently solubilized by papain digestion and is clearly separated from L-leucyl-beta-naphthylamide hydrolase by chromatography on concanavalin A-Sepharose. It probably represents a digestive peptidase, different from the other known peptide hydrolases of the digestive surface of the small intestine.

Aminopeptidases↗
PubMed1974

Functional studies of the parotid and pancreas glands in amyotrophic lateral sclerosis.

Functional studies of the pancreas and parotid glands are reported in 17 patients with amyotrophic lateral sclerosis (ALS). The exocrine function of the pancreas was studied by measuring amylase concentration after stimulation with the endogenous secretin-pancreozymine test (ESP). Under these conditions, the pancreatic amylase concentration in ALS patients was found to be markedly decreased by about 45% when compared with those of healthy control subjects. Different conclusions in the literature about a possible impairment of the exocrine pancreas in ALS patients induced us to study the function of the parotid gland, which has close structural, functional, and physiopathological relationship with the pancreas. Flow rate and bicarbonate concentration of parotid saliva were measured after indirect stimulation (intraoral citric acid) and direct stimulation (pilocarpine). After indirect stimulation, both parotid flow rate and bicarbonate concentration from ALS patients were found to be decreased by about 66% and 70% respectively, when compared with controls. On the other hand, direct stimulation with pilocarpine in ALS patients elicited normal responses in both flow rate and bicarbonate concentration of saliva. It is concluded that the pancreatic and parotid deficiencies observed in ALS patients do not indicate primary disease of these exocrine glands. This interpretation is further emphasized by the results obtained by a sweat test, plasma osmolarity, and sialographic studies. The possibility that the gland impairments observed might be due to modifications of the neuroendocrine mechanisms regulating their secretory activity is suggested.

Adult↗