1,720,986 research outputs found
MTHFR AND RFC-1 GENE POLYMORPHISMS AND THE RISK OF DOWN SYNDROME IN ITALY. AUTHOR'S RESPONSE TO THE COMMENTS BY SCALA ET AL
No full text
A karyological study on populations of Dugesia gonocephala s.l. (Turbellaria: Tricladida)
No full textA karyological analysis was carried out on sexual and fissiparous populations of planarians belonging to the 'Dugesia gonocephala group', collected in localities of the Mediterranean area: Morocco, and Yemen. Euploid (diploid and triploid) chromosome sets are observed in populations reproducing only sexually, whereas hyperdiploid and aneutriploid complements characterize agamous and fissiparous strains. Aneuploidy may occur either associated with an increase in the chromosome number or as a product of rearrangements in numerically balanced chromosome sets. Mitotically unstable B-chromosomes are present in all aneuploid populations. The variety of karyological characteristics encountered is discussed from a cytogenetic and cytotaxonomic standpoint
Analysis of cobalt ferrite nanoparticles induced genotoxicity on human peripheral lymphocytes: comparison of size and organic grafting-dependent effects
No full textWe aimed to detect the potential genotoxic effects of CoFe2O4 particles (CoFe), of different size, by means of the
micronucleus test (MN) in human lymphocytes for the possible use in hyperthermic treatments. CoFe of 5.6 nm (CoFe06)
shows a significant decrease of the cytokinesis blocked proliferation index (CBPI) (pB0.05), in parallel to a significant
increase in the frequency of micronucleated binucleated lymphocytes (BNMN) (pB0.05). For CoFe of 10 mm (CoFe10) a
significant increase in BNMN was found, but any cytotoxic effect. For larger CoFe particles of 120 mm (CoFe120) any
significant effect in both indices was detected. To verify if these effects could be triggered by the release in the medium of
Co2 source, we organically grafted CoFe06 (CoFe6Lig) to analyze if there was a reduction of the Co2-induced toxic
effect. CoFe06Lig showed still a statistically significant genotoxic effect (pB0.05), but 4-fold less than that observed for the
same NP, but ‘naked’
Genotoxicity induced by arsenic compounds in peripheral human lymphocytes analysed by cytokinesis-block micronucleus assay
No full textThis work focuses on the analysis of genotoxic effects on
human peripheral lymphocytes exposed in vitro to different
arsenic (As) compounds by means of the cytokinesis-block
micronucleus assay. The study was carried out by chal-
15 lenging peripheral human lymphocytes with six As compounds
in trivalent or pentavalent forms such as arsenite
(AsIII) and arsenate (AsV) and organoarsenic species such
as monomethylarsonous acid (MMAsIII), monomethylarsonic
acid (MMAsV), dimethylarsinic acid (DMAsV) and
20 trymethylarsine oxide (TMAOV). For AsIII and AsV at concentrations
of 4 and 32 mM, respectively, an increase of
micronuclei (MN) frequency was found. MMAsIII and
MMAsV induced a statistically significant increase of MN
frequency at the dose of 2 and 500 mM, respectively. For
25 DMAsV, no significant increase of MN was observed, although
a decrease of the nuclear division index (NDI) was
evident, indicating a cytotoxic effect. The genotoxic
mechanism of action of MMAsIII was further evaluated
by means of fluorescence in situ hybridization analysis. Due
30 to a higher percentage of centromere-positive MN, MMAsIII
showed a clear aneuploidogenic property. Finally, for
TMAOV no genotoxicity was observed up to 1 mM. These
results show how speciation is important in determining
the genotoxic and cytotoxic effects of As compounds in
35 human peripheral lymphocytes and support the emerging
hypothesis that the induction of aneuploidy could be
a mechanism by which As exerts its carcinogenic
propertie
Genotoxicity assays analysis for carbon nanotubes: Friends or foes? Preliminary results on human peripheral leukocytes ( Review )
No full textPolymorphisms in folate and homocysteine metabolizing genes and chromosome damage in mothers of Down syndrome children
No full textWe recently observed an association between combinations of polymorphisms in the methylenetetrahydrofolate reductase (MTHFR 677C > T or 1298A > C) and reduced folate carrier (RFC-1 80G > A) genes and the risk of a Down syndrome (DS) pregnancy in young Italian women. Others have observed an association between a methionine synthase (MTR 2756A > G) gene polymorphism and the risk of a DS offspring in Italy. Moreover, in a separate study, we observed an increased frequency of both binucleated micronucleated cells (BNMN) and chromosome malsegregation events in peripheral lymphocytes of mothers of DS individuals aged less than 35 years at conception (MDS) in respect to controls. The aim of the present study was to evaluate chromosome damage, measured by means of the micronucleus assay, in peripheral lymphocytes of a group of women (n = 34) who had a DS child in young age ( T and 1298A > C, RFC-1 80G > A and MTR 2756A > G polymorphisms. We observed an increased frequency of BNMN in the MDS group compared to the control group (17.13 +/- 8.31 per thousand vs. 10.28 +/- 4.53 per thousand; P T polymorphism (P = 0.038) was also found. Present results indicate that MDS are more prone to chromosome damage than control mothers; moreover the contribution of folate and homocysteine metabolizing gene polymorphisms seems to have an effect on the baseline frequency of BNMN lymphocytes
Searching for the role and the most suitable biomarkers of oxidative stress in Alzheimer's disease and in other neurodegenerative diseases
No full textThe contribution of oxidative stress to neurodegeneration is not peculiar of a specific neurodegenerative disease, oxidative stress has been
found implicated in a number of neurodegenerative disorders among which Alzheimer’s disease (AD), Parkinson’s disease (PD), amyotrophic
lateral sclerosis (ALS). Even increasing are studies dealing with the search for peripheral biomarkers of oxidative stress in biological fluids
or even in peripheral tissues themselves such as fibroblasts or blood cells. The application of the modified version of the comet assay for
the detection of oxidised purines and pyrimidines in peripheral blood leukocytes results particularly useful if the study requires repeated
blood drawn from the same individual, for instance if a clinical trial is performed with a preventive therapy. Likely damage occurs to every
category of biological macromolecules and we consider, in the context of neurodegenerative diseases, particularly critical the proteic level.
The identification of subjects at risk to develop AD or with pre-pathogenic conditions, the possibility to use “a battery of assays” for the
detection of oxidative damage at peripheral level, together with recent advances in brain imaging, will allow to better address studies aimed
not only to therapeutic purposes but also mainly to primary prevention
Oxidative DNA damage in peripheral leukocytes of mild cognitive impairment and AD patients
No full textAbstract
It is well established that oxidative stress plays a key role in the degenerative neuronal death and progression of Alzheimer’s disease (AD),
although it is not clear if it is the primary triggering event in the pathogenesis of this disorder. Mild cognitive impairment (MCI) is a clinical
condition between normal aging and AD, characterized by a memory deficit without loss of general cognitive and functional abilities. We
performed this study by a comet assay analysis to evaluate the level of primary and oxidative DNA damage in two groups of MCI and AD
patients, compared to healthy controls. Data showed a significantly higher level of primary DNA damage in leukocytes of AD and also of MCI
patients compared to control individuals (average: 2.09±0.79 and 2.47±1.01, respectively for AD and MCI, versus 1.04±0.31 in controls).
Moreover, the amount of oxidised DNA bases (both purines and pyrimidines) was significatively higher in the two groups of patients (AD
and MCI) compared to controls. Our results give a further indication that oxidative stress, at least at the DNA level, is an earlier event in the
pathogenesis of AD
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