1,720,967 research outputs found
Effect of styrene on monoamine oxidase B activity in rat brain.
No full textInhalation exposure to low concentrations of styrene altered MOA-B activity in rat brain
Lymphocyte cholinergic muscarinic receptors: in vivo and in vitro effects of polychlorinated and mathylmercury.
No full textLymphocytes cholinergic muscarinic receptors: in vivo and in vitro effects of the combined exposure to polychlorinated biphenyls and methylmercury.
No full textEthanol selectively interferes with the trophic action of NMDA and carbachol on cultured cerebellar granule cells undergoing apoptosis
No full textIn this study, ethanol promoted apoptotic cell death of cultured cerebellar neurons by selectively inhibiting the neurotrophic effect of NMDA and carbachol. This finding may have implications for the toxicity of prenatal ethanol exposure on the developing cerebellum
Exposure to methylmercury and PCB153 during pregnancy and lactation. Effects on brain and lymphocyte cholinergic muscarinic receptors in rat dams and pups.
No full textValidation of the ELISA test for urinary alpha-amanitin analysis in human Amanita phalloides poisoning
No full textLymphocyte muscarinic receptors and platelet monoamine oxidase-B as biomarkers of CNS function: effects of age and gender in healthy humans
No full textLymphocyte cholinergic muscarinic receptors (MRs) and platelet monoamine oxidase-B (MAO-B) activity are considered surrogate markers of the same parameters in the central nervous system. Lymphocyte MR binding and platelet MAO-B activity were measured in a consistent number of healthy human adults and analysed according to gender and age. The mean value±S.D. of MR binding neither differed between males (12.2±10.0 fmol/106 cells, range: 0.5–37.9, n = 86) and females (10.7±9.7 fmol/106 cells, range: 0.5–39.7, n = 69) nor among age groups. MAO-B activity was significantly higher in women (geometric mean: 11.3 nmol/mg protein/h, with 65% of values from 7.3 to 17.6; n = 43), than in men (7.7 nmol/mg protein/h, with 65% of values from 4.5 to 13; n = 95). Males aged 56–66 years displayed a higher, though not statistically significant, basal enzyme activity than younger subjects. Altogether these data indicate gender-related differences in MAO activity, but not in MR binding, and inter-individual differences in the basal values of both peripheral blood markers in healthy subjects
Lymphocyte cytochrome c oxidase, cyclic GMP and cholinergic muscarinic receptors as peripheral indicators of carbon monoxide neurotoxicity after acute and repeated exposure in the rat
Full text linkChanges in cerebral cytochrome oxidase (COX) activity, nitric oxide (NO)–cyclic GMP (cGMP) pathway and cholinergic muscarinic
receptors (MRs) have been reported in rodents acutely exposed to carbon monoxide (CO). These endpoints measurable in lymphocytes may serve as peripheral markers of CO neurotoxicity. The early and delayed effects of repeated and acute in vivo CO inhalation were investigated on COX activity, cGMP formation and MR binding in rat brain and lymphocytes to assess whether each endpoint was similarly affected both centrally and peripherally. Male Wistar rats either inhaled 500 ppm CO, 6 h/day, 5 days/week, 4 weeks (repeated exposure) or 2400 ppm, 1 h (single exposure). Neither treatment altered brain or lymphocyte COX activity 1 and 7 days post-treatment. Also ineffective were repeated and acute CO treatments towards 3H-quinuclidinyl benzilate (QNB) binding to MRs in cerebral cortex, hippocampus, striatum, cerebellum (respective controls, meanTS.D.: 171T45, 245T53, 263T14 and 77T7 fmol/mg protein) and lymphocytes (24T10 fmol/million cells) at the same time points. In lymphocytes control cGMP levels averaged 1.98T0.99 pmol/mg protein under basal conditions, and 3.94T0.55 pmol/mg protein after NO-stimulation. One day after chronic treatment cessation, the CO-treated group displayed about a 50% decrease in both basal and NOstimulated cGMP values, which persisted up to 7 days after, compared to air-exposed rats. Acutely, CO caused a delayed enhancement (+140%) of NO-induced activation of soluble guanylate cyclase. The finding that the NO–cGMP pathway is a target for the delayed effects of CO in peripheral blood cells is in accordance with our data in brain. In vivo exposure to carbon monoxide causes delayed impairment of activation of soluble guanylate cyclase by nitric oxide in rat brain cortex and cerebellum
Methylmercury interaction with lymphocyte cholinergic muscarinic receptors in developing rats
No full textCerebral cholinergic muscarinic receptors (MR) have been suggested as one of the sensitive biochemical endpoints of the central nervous system altered by developmental exposure to the widespread seafood contaminant methylmercury (MeHg). In adult rats, MeHg has been shown to alter MR binding both in the brain and lymphocytes, supporting the use of MR in blood cells as a surrogate marker of
CNS changes. The effects of MeHg have been evaluated on rat lymphocyte MR binding (using [3H]QNB as specific muscarinic ligand) in vivo (after perinatal exposure) and in vitro. For comparison, in vitro studies were also performed on human lymphocytes. Exposure to 1mg MeHg/kg/day during pregnancy and lactation (from GD7 to PND7) significantly enhanced lymphocyte MR density in both adult and young rats 21 days after delivery, with a more pronounced effect in the mothers (Bmax increase of 139%) than in the male offspring (+49%) and female offspring (+73%) as compared with their respective controls (3374, 4178, and 3774 fmol/million cells), in accordance with the higher Hg levels detected in the adult blood (11.372.2 mg/mL) than in pups (1.370.4 mg/L in both genders).
A lower MeHg dose (0.5 mg/kg/day) was without any effect on lymphocyte MRs. In in vitro studies, MeHg was an almost equipotent
inhibitor of 3H-QNB binding to rat and human lymphocyte MRs (IC50 values were 4.170.29, 5.270.51, and 5.070.9 mM for total rat
lymphocytes, rat T lymphocytes, and total human lymphocytes, respectively). Notably, the IC50 values for MeHg to lymphocyte MRs
were comparable to the Hg levels reached in blood (5–50 mM) of the PND21 rats exposed to MeHg.
The finding that the MR binding is a target for the effects of MeHg in peripheral blood cells is in accordance with our previous data in
brain [Coccini et al., 2006. Effects of developmental co-exposure to methylmercury and 2,20,4,40,5,50-hexachlorobiphenyl (PCB153) on
cholinergic muscarinic receptors in rat brain. Neurotoxicology, in press], and supports the use of this peripheral endpoint as a biomarker of MeHg-induced cerebral muscarinic alterations. The similarity of MeHg IC50 binding data between human and rat in peripheral tissues suggests the possible application of such biomarker to humans exposed to environmental chemical
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