Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Measures of genotoxicity included the determination of the frequencies of chromosomal aberrations (CA), sister-chromatid exchange (SCE), HPRT mutations (variant frequency, VF) and the measurement of UV-induced unscheduled DNA-repair synthesis (UDS).
|
20193773 |
2010 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The no observed adverse effect level (NOAEL) for chromosome aberrations and HPRT mutations was 1.794 mg/m(3) (0.812 ppm)--the mean exposure level for the highest exposed worker group in this initial study.
|
16949064 |
2007 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Mrad9(-/-) cells demonstrated a marked increase in spontaneous chromosome aberrations and HPRT mutations, indicating a role in the maintenance of genomic integrity.
|
15282322 |
2004 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Genetic damage induced by in vitro irradiation of human G0 lymphocytes with low-energy protons (28 keV/microm): HPRT mutations and chromosome aberrations.
|
12816523 |
2003 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The acquired data on single-strand breaks in DNA (SSBs), frequency of chromosomal aberrations and HPRT mutant frequency in peripheral blood lymphocytes were compared to the results on genotyping of some of the xenobiotic-metabolising enzymes (CYP1A1, CYP2E1, epoxide hydrolase and GSTM1, GSTP1 and GSTT1).
|
11535253 |
2001 |
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
The most often studied genotoxicity endpoints have been selected for inclusion in this document and they are structural and numerical chromosomal aberrations assessed using cytogenetic methods (classical chromosomal aberration analysis (CA), fluorescence in situ hybridisation (FISH), micronuclei (MN)); DNA damage (adducts, strand breaks, crosslinking, alkali-labile sites) assessed using bio-chemical/electrophoretic assays or sister chromatid exchanges (SCE); protein adducts; and hypoxanthine-guanine phosphoribosyltransferase (HPRT) mutations.
|
10913908 |
2000 |
Congenital chromosomal disease
|
0.100 |
Biomarker
|
group |
BEFREE |
Biomarkers of exposure (substance or its metabolites in biological fluids, urinary mutagenicity, protein and DNA adducts) and of effects (chromosome aberrations (CAs), sister chromatid exchanges (SCEs), micronuclei (Mn), COMET assay, HPRT mutants) have been evaluated according to different genotypes (or phenotypes) of several activating/detoxifying metabolic activities.
|
11018745 |
2000 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Blood samples from normal male and female subjects and from patients with X and Y chromosome disorders (45,X and 47, XXY) have been tested by QF-PCR with the X22 polymorphic pentanucleotide (12 alleles) together with the HPRT and P39 markers.
|
10590424 |
1999 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
To illustrate the problem, a brief review of studies using well validated techniques (chromosome aberrations and hprt gene mutation) to elucidate genotoxic effects of cigarette smoking is presented.
|
9685705 |
1998 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
Frequencies of HPRT mutants (MFs), chromosomal aberrations with or without gaps (CA+; CA-), aberrant cells (AC), micronuclei (MN), sister-chromatid exchanges (SCEs) and cells with high frequencies of SCEs (HFCs) were measured in lymphocytes collected from 46 workers occupationally exposed to styrene and dichloromethane (DCM = methylene chloride).
|
7523909 |
1994 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
All samples were analyzed for HPRT mutants (MFs), chromosomal aberrations (CAs), micronuclei (MN) and SCEs.
|
1719390 |
1991 |
Congenital chromosomal disease
|
0.100 |
GeneticVariation
|
group |
BEFREE |
By using hypoxanthine guanine phosphoribosyltransferase (hprt) gene alterations and chromosome aberrations as in vivo cellular markers, human T, NK, and B cells originating from a single stem cell have been successfully cloned from the peripheral blood of an atomic bomb survivor from Hiroshima.
|
2784484 |
1989 |