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Biomedical subjects

A Mutti

Publications and source records attributed to A Mutti.

154 records · Page 9Linked to original sources
PubMedDate not supplied

Serum prolactin in subjects occupationally exposed to manganese.

To evaluate whether or not occupational exposure to manganese (Mn) affects basal levels of serum prolactin (PRL), a cross-sectional study was carried out in 31 occupationally-exposed workers, aged 39.2 years (DS 7.9) exposed to manganese (Mn) dusts for 14.5 years (range: 5 to 29 years) in a ferroalloy producing plant. Thirty-four industrial workers not exposed to neurotoxic chemicals and of comparable age composed the control group. Airborne Mn concentrations in dusts of the furnace area ranged 210 to 980 micrograms/m3, which is below the current American Conference of Governmental Industrial Hygienists (ACGIH)-recommended threshold limit value-time weighted average (TLV-TWA) of 1 mg/m3. Manganese concentrations in blood Mn (MnB) and in urine (MnU) were significantly higher in Mn-exposed workers as compared to control workers. The Mn-exposed workers showed significantly higher serum prolactin (PRL) levels with the geometric mean (GM) being 9.77 ng/ml with a geometric standard deviation (GSD) of 1.69 as compared to controls (GM 4.65 ng/ml, GSD 1.78, p < 0.001). Serum PRL was negatively related to age and positively correlated with both MnB and MnU. Dose-effect relationships were still significant in partial correlation analysis after control for age. The prevalence of abnormally high PRL values was consistent with a dose-response relationship. The observed increase in serum PRL among Mn-exposed workers suggests an impairment of tonic inhibition by tubero-infundibular dopaminergic neurons. The correlation between PRL and both MnB and MnU in samples collected at least 48 h from the last exposure suggests that such indices provide an estimation of the target dose.

Adult↗
PubMedDate not supplied

Dopamine (DA) metabolism in PC12 cells exposed to manganese (Mn) at different oxidation states.

The present study was aimed at assessing the role of Mn valency state in Mn-induced changes in DA metabolism by PC12 cells. Mn(ll)Cl2, Mn(lll)Acetate, and Mn(IV)O2 were used for these experiments. PC12 cells were incubated for 3, 24 and 72 hours to Mn nominal concentrations ranging from 10-8 to 10(-4) M in 24-well plates containing 2 x 10(5) cells/well. Supernatants and cellular materials were then separated and immediately processed for the analysis of dopamine (DA), and its metabolite 3,4-di-hydroxy-phenylacetic acid (DOPAC). Lactate dehydrogenase (LDH) activity and MTT cleavage were measured as indices of cell death. In parallel experiments, Mn-containing medium (10(-5) M) was removed and cells incubated for further periods with Mn-free medium to evaluate the reversibility of observed changes. At the end of the experimental periods, none of Mn-exposed cultures showed appreciable reduction in cell viability as compared to their respective controls. After exposure to Mn(II) and Mn(III), irreversible and dose-dependent decreases in the medium but not in intra-cellular DA were apparent. Indeed, 10(-4) M Mn(II) caused the disappearance of DA and DOPAC from the medium. The same effect was caused by 10(-5) M Mn(III), the dose-effect relationship being shifted towards lower dose levels. Mn(IV) induced a parallel and dose-dependent decrease of DA and DOPAC concentrations in both intra- and extra-cellular compartments. Such an effect was reversible after removal of Mn from the medium. Multiple interferences on DA metabolism are caused by Mn. Mn(II) and Mn(III) seem to block DA secretion without affecting DA turnover rate. Mn(IV) seems to cause DA depletion and aspecific (secondary) changes in secretion rates. Further studies are necessary to understand the mechanisms underlying the differential effects of various Mn compounds on DA metabolism.

Animals↗
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Peripheral markers of neurochemical effects among styrene-exposed workers.

Monoamine oxidase B (MAO-B) activity in platelets, serum dopamine-beta-hydroxylase (DBH) activity, and serum prolactin (PRL) were measured during a cross-sectional investigation in workers occupationally exposed to styrene. The study group consisted of 53 workers (33 men and 20 women) employed for 9.3 years on average (range 1-22) in reinforced plastics plants. Sixty industrial workers with no known exposure to chemicals and comparable as to age, sex and confounding variables were recruited as controls. The activities of MAO-B in platelet-rich plasma and of DBH in serum from exposed and control subjects were measured within the same run, using methods based on the liquid-chromatographic determination of the reaction products. Serum PRL was determined by both EIA and RIA. Blood samples had been collected between 8:00 and 9:00 a.m. A lower DBH activity was found in exposed as compared to control workers (GM: 7.25 U/ml serum vs. 10.11 U/ml serum; p < 0.01), whereas MAO-B activity was significantly lower in a heavily exposed subgroup (10.1 vs. 13.8 U/10(7) platelets; p = 0.05), but not in the whole sample (p = 0.07). Serum PRL was higher both in male (GM: 8.90 ng/ml vs. 6.05 ng/ml; p < 0.01) and female (GM: 12.6 ng/ml vs. 9.33 ng/ml; p < 0.05) styrene-exposed workers as compared to their respective controls. Dose-response relationships were found for abnormally low DBH and abnormally high PRL values, with a threshold occurring at metabolite levels corresponding to 8h-TWA styrene concentrations in air around 25 ppm. In summary, this study shows that long-term exposure to relatively low levels of styrene can affect DBH activity and basal serum PRL. Owing to its sensitivity, PRL is a useful biomarker to show impairments of dopaminergic control on pituitary secretion. Since DBH is expression of catecholamine secretion, its decreased activity could represent an indirect index of altered turnover rate of the physiological substrate (i.e.dopamine) at the neuronal level. However, a direct interference by styrene metabolites on enzyme activity cannot be ruled out. Platelet MAO-B activity seems to be less sensitive to styrene exposure.

Adult↗
PubMedDate not supplied

Pilot study of peripheral markers of catecholaminergic systems among workers occupationally exposed to toluene.

In a pilot study, serum dopamine beta-hydroxylase (DBH), platelets monoamine oxidase type B (MAO B) activities and basal plasma prolactin (PRL) were measured, among 10 workers occupationally exposed to toluene and 10 control subjects, preceding and immediately following vacation. Six exposed subjects were employed in an adhesive tape making industry and 4 in a paint making industry. Their median basal levels of urinary hippuric acid were 0.44 mmole/mmole creatinine (cr) (range 0.23-1.97) and 0.18 mmole/mmole cr (range 0.15-0.19) respectively, the second to last morning of the work week, preceding vacation. The level of basal urinary hippuric acid among the control group was 0.26 mmole/mmole cr (range 0.03-0.38). The workers from the adhesive tape plant reported a significantly higher number of symptoms experienced frequently (Kruskal, Wallis, p < 0.05). On a group basis, serum DBH was lowest among the workers from the adhesive tape plant, who had the highest levels of basal urinary hippuric acid. In addition, a negative relation was observed between hippuric acid and serum DBH, preceding and following vacation (Rho = -0.46, p = 0.05; Rho = -0.51, p = 0.03). The observed changes in serum DBH activity are consistent with its decrease in human, following long-term exposure to styrene, another aromatic hydrocarbon. The findings of this pilot study, on a limited number of individuals suggest that DBH may be a sensitive peripheral bioindicator. Further studies of larger groups should be done to confirm the decrease in serum DBH activity with toluene exposure and explore whether this alteration is related to the neurotoxic impairments associated with exposure.

Adult↗
PubMedDate not supplied

Predictive validity of the Q16 questionnaire: a comparison between reported symptoms and neurobehavioral tests.

The correspondence between the answers to the Q16 questions regarding memory and attention-concentration and relevant neurobehavioral performance test scores has been evaluated. The sensitivity, specificity and diagnostic validity of Q16 have been assessed, taking the relevant neurobehavioral test score as a reference diagnostic criterion, the lower quartile of performance being considered as a poor response. The group under study consisted of 74 volunteers (24 females), aged 40 years on average (SD:7.5) and recruited among styrene-exposed workers and healthy controls. The test battery included the logical memory (short- and long-term) and the verbal learning (short- and long-term) tests of the Wechsler Adult Intelligence Scale (WAIS). The answers to the Q16 questions were poorly related to the performance: self-perceived forgetfulness showed a limited agreement with the long-term logical memory test (r=-0.23, p<0.05). The number of false negatives (no symptom but low test scores) was generally high, giving rise to a very low sensitivity of the questionnaire, despite a relatively high specificity. Accordingly, the positive diagnostic validity was low (<30%), whereas the negative diagnostic validity was high (>80%). Different methods used to investigate subtle neurological changes give rise to inconsistencies between self-perceived disturbances and objective measurements of relevant functions. Owing to its low sensitivity and positive diagnostic value, the Q16 cannot be recommended as a screening tool among workers occupationally exposed to neurotoxic chemicals.

Adult↗
PubMedDate not supplied

A case-control study of occupational and environmental risk factors for Parkinson's disease in the Emilia-Romagna region of Italy.

A questionnaire-based case-control study was carried out on 86 patients with neurologist-confirmed idiopathic Parkinson's disease (PD) and 86 controls similar in sex and age. The control group was recruited in outpatient specialist centers of the same University Hospital (glaucoma, psoriasis vulgaris, essential arterial hypertension and renal diseases). Exposure was defined as occupational or residential contact with a given factor for at least 10 consecutive years prior to the onset of PD. Smoking habits were defined by exclusion of those subjects who never smoked. The following risk factors were identified: cranial trauma (OR: 2.88; 95% CI: 0.98-8.49), well water use (OR: 2.78; 95% CI: 1.46-5.28) and occupational exposure to industrial chemicals (OR: 2.13; 95% CI: 1.16-3.91). Among industrial chemicals, only organic solvents were identified as significant risk factors for PD (O.R. : 2.78, 95% C.I. : 1.23-6.26). Whereas no exposure to neurotoxic metals occurred among controls, making the assessment of the O.R. impossible, exposure pesticides and herbicides was similar in the two groups (O.R. : 1.15; 95% C. : 0.56-2-36). Smoking habits was negatively associated with PD (OR: 0.41; 95% CI: 0.22-0.75), confirming the "protective" role of tobacco smoking suggested by many studies. As a whole, these results support the role of environmental factors in the etiology of PD.

Aged↗