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G Ugazio

Publications and source records attributed to G Ugazio.

At least 37 records · Page 2Linked to original sources
PubMed1988

Experimental studies on the toxicity of Ferula communis in the rat.

The study of two chemically characterized varieties of Ferula communis showed that only plants containing prenylated coumarins are toxic. The contrasting data on the toxicity of Ferula communis most probably raised from the use of chemically uncharacterized specimens. Among the constituents of the toxic variety, both ferulenol, a 4-hydroxycoumarin derivative, and ferprenin, a pyrane (3,2-c) coumarin derivative, affected blood clotting. No hepatotoxicity was elicited by these two compounds.

Animals↗
PubMed1987

Effects of the chronic administration of sodium selenite on rat testes.

Testis structure and functions were monitored in male Wistar rats chronically exposed to various levels of sodium selenite (Na2SeO3) in drinking water (4, 8 or 16 ppm). The most remarkable testicular changes were observed in the 16 ppm group: intertubular oedema, oligospermia, scattered foci of degenerated spermatids were found. In addition, marked changes in several specific enzymes of testicular cells occurred along with a significant reduction of mean-tubular-diameters, mean-tubular-areas and mean-tubular-perimeters. These results clearly demonstrate a testicular involvement during chronic exposure of the rat to selenium.

Animals↗
PubMed1986

A model for monitoring changes in liver function.

An experimental model for monitoring rat liver function during protracted exposure to hepatotoxic agents is proposed. Owing to their invasiveness, the models usually employed are appropriate for studying the mechanism of action of toxic substances, but do not allow the liver situation to be followed over the course of time. The need to sacrifice animals to determine liver triglycerides-one of the key parameters in the progress of toxic damage- reduces the possibility of following such progress in the same animals. This study describes the testing of a model for monitoring three basic parameters of liver injury: cytolysis, steatosis and metabolic deficiency of the liver. CCl4 has been chosen as model-hepatotoxin. Steatosis is determined by evaluating the triglyceride content of small specimens of liver, obtained through open-field biopsies, which appear to be representative of the whole liver. Fatty liver is paralleled by the block in Triton-induced hypertriglyceridaemia. Determination of serum triglycerides derives from a very poorly invasive technique which can be repeated several times. The combination of these tests with the assessment of both the cytolysis (ALT and SDH release into the circulation) and the impairment of the efficiency of liver microsomal enzymes (TMO clearance), seems to offer a reliable experimental procedure in predicting the hepatotoxic effect of xenobiotics.

Animals↗
PubMed1985

Hepato- and neuro-toxicity by ethylenthiourea.

Thyrotoxicity of Ethylenthiourea (2-imidazolidinethione) (ETU) is well known: this paper examines the extent to which ETU alone may damage certain non-thyroid tissues, and the possible enhancement of its effects through synergism when it is taken with substances employed for medical or alimentary reasons. It was found that the lethality of ETU is augmented by accumulation of fractionated doses, particularly in male as opposed to female rats. When accompanied by ethanol, its harmfulness is increased, whereas phenobarbital provides a certain degree of protection. Liver secretion of triglycerides is greatly impaired (delta % = -31) by acute administration, which results in steatosis. This is not observed during subacute administration. Liver microsomal cytochrome P450 is significantly reduced (delta % = -32) after a long term administration. The 30 week treatment leads to a form of "selection". Some animals die (28.6%), whereas others survive despite: i) prolonged failure to put on weight, ii) alopecia (80% loss of hair), iii) severe conjuntivitis, iv) blepharitis, v) peripheral nervous system distress. These findings underscore the importance of investigating the relation between hazardous compounds and possible potentiating factors, on the one hand, and inclusion of organs not yet recognized as targets, on the other hand, when setting tolerance limits for ambient pollution.

Animals↗
PubMed1984

Effects of metal ions and CCl4 on sea urchin embryo (Paracentrotus lividus).

The determination of embryotoxicity is an experimental tool for detecting the risks of environmental pollutants. In this study, fertilized eggs of sea urchin have been observed morphologically during exposure to heavy metal salts or carbon tetrachloride, with the purpose of testing possible differences in toxicity of various classes of poisons. Mercuric chloride is the most active salt, still harmful at 0.25 x 10(-6) M, while potassium dichromate, cadmium chloride and lead nitrate block embryo development at concentrations ranging between 0.25 x 10(-4) and 0.25 x 10(-5) M. Carbon tetrachloride per se does not affect the gastrulation at concentrations up to 3,520 ppm, and fails in potentiating the toxicity of the studied metal salts. The selective susceptibility of the development phases of sea urchin embryos to different compounds renders this simple morphological study a sensitive and reliable model for predicting the toxicity of environmental pollutants.

Animals↗
PubMed1983

Impairment of erythropoiesis in rats exposed to environmental pollutants.

The extent to which halogen compounds interfere with erythropoiesis is still unclear. This paper reports an evaluation of the effect of repeated exposure to carbon tetrachloride (CCl4) in air on red blood cell (RBC) creatine concentration. Creatine is neither synthetised nor metabolised in circulating RBC and decreases over the lifespan of red cells. It can thus be taken as a reliable indicator of mean RBC age, and hence of cell viability and bone marrow efficiency. Following inducement of hemolysis with phenylhydrazine (PHH) to stimulate erythropoiesis, creatine levels rose in the controls. This increase was significantly less in the CCl4-treated animals. It is not yet certain whether this inhibition reflects impaired marrow efficiency, enhanced RBC destruction in the marrow, or block of the release of mature RBC. The fact that such inhibition takes place, however, is of importance as a predictive factor in environmental toxicology, since it appears before changes in other blood parameters or signs of liver toxicity are observed.

Animals↗
PubMed1982

Bromsulphalein (BSP) kinetics in the rat: a new approach in evaluating experimental hepatotoxicity.

An animal model for the identification and definition of toxic liver damage, based on the investigation of the BSP metabolism in the rat is proposed. Different hepatotoxins can induce specific functional alteration on the different steps of the BSP hepatobiliary transport, mainly the uptake by hepatocytes and the biliary excretion. Removal curves of BSP from the plasma compartment as well as the biliary secretion were evaluated in rats treated with either alpha-naphthylisothiocyanate (ANIT) for metabolic cholestasis, or with carbon tetrachloride (CCl4) for fatty infiltration and necrosis of the liver. The data were compared with those obtained with untreated rats and with animals submitted either to complete or incomplete mechanically induced cholestasis. Our results lead to the conclusion that a satisfactory discrimination among different types of liver damage may be obtained when only two plasma parameters of BSP metabolism are considered: the disappearance rate for the early 5 min (K), and 15-min plasma BSP retention (R15). The model is proposed as a suitable tool for the evaluation of experimental hepatotoxicity in living rats giving a characterisation of the functional alteration and a measure of liver impairment.

1-Naphthylisothiocyanate↗
PubMed1982

Mechanism of protection against carbon tetrachloride toxicity. I. Prevention of lethal effects by partial surgical hepatectomy.

Both partial surgical hepatectomy and a challenge with a small dose of CCl4 depress the metabolism of xenobiotics in the liver. In fact, hepatocytes become provided with metabolic activity rates which are peculiar of either embryo or newborn rat liver. These experiments have shown that partial surgical hepatectomy prevents rats from death caused by otherwise lethal doses of CCl4. At the same time, sham-operated animals survive to a limited extent after a large dose of the halogen compound. Investigations carried out on the metabolic efficiency of liver microsomes, both in vito and in vivo, clearly demonstrate that the preventive effect against CCl4 depends mainly on the impaired metabolic activity of endoplasmic reticulum.

Aminopyrine N-Demethylase↗
PubMed1982

Mechanism of protection against carbon tetrachloride toxicity. II. Lethality in rats fed a polyunsaturated fatty acid deficient diet.

A PUFA-deficient diet causes deficiency symptoms and alters the fatty acid pattern in liver microsomal lipids. However, CCl4 lethality and sleeping time remain unchanged while the hepatic level of cytochrome P450 is only slightly lowered by the dietary regimen. In accordance, the amplitude of double bond shifting in microsomal lipids is far from being depressed in animals deprived of the peroxidative substrate. In fact, the experimental treatment does not impair intestinal absorption, liver uptake and metabolism of CCl4 given orally. Finally, both in vitro and in vivo peroxidative challenge of arachidonic acid content in hepatic microsomes causes comparable alterations of this parameter, whatever the initial fatty acid pattern following the dietary regimen. These findings provide evidence excluding an influence of the fatty acid composition of the diet on the severity of damages due to halogen-alkane exposure.

Animals↗
PubMed1980

Strain- and sex-linked effects of dietary polyunsaturated fatty acids on tumor growth and immune functions in mice.

In the present paper, we studied the influence of different levels of dietary polyunsaturated fatty acids (PUFA) on the immune system and tumor growth in young mice. Female BALB/c mice fed a PUFA-rich diet display an enhanced body growth, proliferative response to mitogens in vitro, and rate of growth of a spontaneous transplantable adenocarcinoma as compared to PUFA-poor diet-fed females. Such effects are, however, limited by sex and strain background genes located outside the H-2 complex. In effect, the influence of dietary PUFA content is evident in female but not in male BALB/c mice. Moreover, in female DBA/2 mice with the same haplotype (H-2d) of the major histocompatibility complex as that of BALB/c mice, low dietary PUFA determines a reduced tumor growth only, but it does not affect body growth and proliferative response to mitogens in vitro.

Adenocarcinoma↗