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Biomedical subjects

A R Volpe

Publications and source records attributed to A R Volpe.

At least 181 records · Page 10Linked to original sources
PubMedDate not supplied

Neurobehavioral functions, serum prolactin and plasma renin activity of manganese-exposed workers.

Objective of this study was to assess effects of manganese (Mn) exposure on 56 workers employed in a Mn welding workshop of a machine building factory in Taiyuan (Shanxi Province, P.R. China) for a mean period of 16.1 years. The mean air Mn level in the workshop was 138.4 microg/m3. Neurobehavioral Core Test Battery (NCTB), including the Profile fo Mood States, (POMS), was performed. Blood pressure (BP) increase following immediate stand-up (BP-IS), serum prolactin (PRL) and plasma renin activity (PRA) in supine position were also determine. Most of the NCTB scores of the Mn-exposed workers were lower than those of controls, while the POMS scores were higher, indicating a Mn-induced impairment of neurophysiological functions and a deflection of mood towards negative emotion states. PRL values of the Mn-exposed workers were higher than those of the controls. BP-IS of Mn-exposed workers was significantly lower than that of the controls. PRA of the same workers was augmented more that 200%. In the Mn-exposed workers, the higher PRL values are possibly due to a reduced inhibitory effect on pituitary lactotrope cells by the tubero-infundibular dopamine system; the decreased BP-IS was referred to imbalance between the sympathetic and parasympathetic activities, whereas the higher basal PRA was thought to depend on neuroendocrine changes (including increased central sympathetic tone) and/or on a direct effect of Mn on renal juxta-glomerular cells. On the whole, this study demonstrates that occupational Mn exposure is responsible for neurobehavioral changes coexisting with alterations of neuroendocrine and humoral systems.

Adult↗
PubMedDate not supplied

Clastogenic but not apoptotic effects on human artery endothelial cells by concentrations of inorganic lead inhibiting their nitric oxide production.

Human coronary artery endothelial cells (HCAEC 5156) were cultured as monolayers and exposed to concentrations of lead (as acetate, Pb) in the culture medium similar or lower than those commonly found in the blood of human beings occupationally or environmentally exposed to this element. Only at the concentration of 200 ng/mL, Pb reduced growth rate of HCAEC 5156 cells starting from the 3rd day and up too the 5th day of incubation. On the other hand, Pb (0.2, 2 and 200 ng/mL) increased concentration-dependently micronuclei formation in binucleated HCAEC 5156 cells, as it was shown by the cytokinesis-blocked micronucleus assay (CMBN assay) carried out after 48 hours of exposure to the metal. However Pb was unable, at all the above concentrations to induce apoptosis in the HCAEC 5156 cells following a 48 hour-exposure, as shown by an electorphoretic apoptotic DNA fragmentation test. Moreover, Pb (2 and 200 ng/mL) reduced significantly the concentration of nitric oxide (NO, determined analytically as L-citrulline) in both culture medium and cytosol of HCAEC 5156 cells following a 7 day-exposure to the element. Results were discussed also in relation so evidences of other studies reporting genotoxic and/or apoptotic effects of Pb on various cell types at very elevated dosages of concentrations. The observed clastogenic effects of Pb were explained through a series of mechanisms involving interactions between oxygen reactive species and NO and/or reduced NO synthesis in the endothelium, thus leading to a depressed NO bioavailability. This research first shows that Pb is provided with clastogenic but not apoptotic effects on cultured human endothelial cells. It was emphasized that such effects are induced by Pb concentrations similar to those commonly found in blood and tissues of laboratory animals showing Pb induced cardiovascular and/or neuropsychological alterations.

Apoptosis↗
PubMedDate not supplied

Shock induction by arterial hypoperfusion of the gut involves synergistic interactions between the peripheral enkephalin and nitric oxide systems.

To determine whether critical splanchnic artery hypoperfusion can provoke systemic shock and to identify the roles of the peripheral opioid and nitric oxide (NO) systems in this process, various degrees of superior mesenteric artery hypoperfusion (SMA-H) were produced in anesthetized adult rabbits (n=40), and hemodynamic and metabolic indices were measured. Metabolic acidosis and irreversible hypodynamic shock occurred with SMA-H at levels representing 25-20% of mean baseline SMA blood flow. In 112 other rabbits subjected to SMA-H at 20% (SMA-H20%), we studied plasma NO and enkephalin (ENK) levels, cardiovascular reactivity to selected physiological agonists, effects of ENKs on plasma NO levels, and effects of peripheral opioid receptor blockade and inducible NO synthase (iNOS) inhibition. SMA-H20% progressively increased systemic blood levels of NO and ENKs. Exogenous ENK administration accentuated SMA-H20%-induced increases in plasma NO levels, and their cardiovascular depressing effects were significantly greater when they were administered during SMA-H20% (vs. administration under baseline conditions). Selective blockade of cardiovascular delta-opioid receptors improved hemodynamics, prevented shock irreversibility and reduced plasma NO levels; similar effects were obtained by selective iNOS inhibition. These findings demonstrate that critical arterial hypoperfusion of the gut can induce hypodynamic systemic shock through ENK-induced hyperactivation of cardiovascular delta-opioid receptors, which leads to increased plasma levels of NO related in part to increased iNOS activity. Since pronounced splanchnic artery hypoperfusion occurs in all advanced systemic shock states, selective delta-opioid receptor antagonists and/or iNOS inhibitors may prove to be useful in improving shock hemodynamics and metabolic derangements and/or preventing progression toward irreversibility.

Animals↗
PubMedDate not supplied

Clinical effect of a triclosan-containing dentifrice on plaque and gingivitis: a six-month study.

A total of 294 adult male and female subjects completed a 6-month, double-blind clinical trial designed to evaluate the effects of a dentifrice which contained 0.3% triclosan in conjunction with 2% of a methoxyethylene/maleic acid copolymer in a 0.243% sodium fluoride/silica base, relative to a control dentifrice, on supragingival plaque accumulation and gingivitis. Plaque and gingivitis were scored after 3 and 6-month use of the assigned dentifrice. At the end of the study, the triclosan group showed an average reduction, relative to the control group, of 12% in plaque accumulation and 20% in gingivitis. Both were statistically significant at p < or = 0.0001. The effect of the triclosan dentifrice was most pronounced on the more severe manifestations of plaque and gingivitis. The improvement in the gingival parameters at 6-months relative to the control dentifrice was statistically significant at p < or = 0.0001. It was concluded that the twice-daily use of the triclosan-containing dentifrice resulted in significant reduction in supragingival plaque formation and a significant improvement in gingival health without the presence of any extrinsic staining or objectionable taste.

Adolescent↗
PubMedDate not supplied

Effect of a dentifrice containing triclosan and a copolymer on plaque formation and gingivitis.

A total of one hundred twenty-one (121) adult male and female subjects completed a 6-month, double-blind clinical study comparing the effect on supragingival plaque formation and gingivitis of a dentifrice containing 0.3% Triclosan and 2.0% of a copolymer of methoxyethylene and maleic acid to a placebo dentifrice. Both the Triclosan/copolymer and placebo dentifrices contained 0.243% sodium fluoride in a silica base. Subjects were stratified into two balanced groups according to baseline plaque and gingivitis scores. They then received an oral prophylaxis and were assigned to use either the Triclosan/copolymer dentrifrice or the placebo dentifrice for the next 6 months. Subjects were evaluated for supragingival plaque formation and gingivitis after 3 and 6 months' use of the dentifrices. After 6 months, the Triclosan/copolymer dentifrice was shown to provide a 32.32% statistically significant reduction (99% level of confidence) in supragingival plaque formation, as compared to the placebo dentifrice. Also, after 6 months, the Triclosan/copolymer dentifrice was shown to provide a 25.64% statistically significant reduction (99% level of confidence) in gingivitis, as compared to the placebo dentifrice. It thus can be concluded from this clinical study that the twice daily use of the dentifrice containing 0.3% Triclosan and 2.0% of a copolymer in a 0.243% sodium fluoride/silica base provides statistically significant reductions in both supragingival plaque formation and gingivitis.

Adult↗
PubMedDate not supplied

Vanadate and cardiovascular system.

Rats were given 1, 10, 40, or 100 ppm of vanadium in drinking water for seven months, while rabbits received 1 ppm of vanadium (as sodium metavanadate, NaVO3) in drinking water for twelve months. Rats developed arterial hypertension through complex effects of vanadium on central neurogenic pathways, central and periferal catecholaminergic mechanisms, specific autacoidal systems (kallikrein-kinin, reninangiotensin-aldosterone, enkephalin ones), and effectors (vessels and heart). The above effects of vanadium were in part confirmed in the rabbits which, however, did not show arterial hypertension since the increase of vascular resistance was counteracted by a reduction of both cardiac inotropism and cardiac output. Vanadium was accumulated in tissues as vanadyl; higher levels were found in the bone and in the kidney, but relevant amounts were determined in aorta, heart and brain. There was evidence, in the rabbits, that vanadium reduces synthesis and/or release of nitric oxide, the endothelium-derived vasodilating factor, likely through a reduced formation from bradykinin. The functional, analytical and morphological results obtained in this study show that chronic exposure to vanadium induces arterial hypertension by mechanisms only in part related to the levels and times of exposure, and to the species.

Animals↗