Any fluid chromatography conjunction bulk spectrometry way of semiquantitative screening process associated with cell acyl-CoA.

d Huh6 were suitable for the assessment of PA-induced genotoxicity. Selected PAs confirmed previously published potency rankings in the micronucleus assay. In HepG2 cells, the crosslinking activity was related to the ester type, which is a first report of PA mediated effects in the comet assay.Acetaldehyde (AA) has been classified as a probable human carcinogen by the International Agency for Research on Cancer (IARC, WHO) and by the US Environmental Protection Agency due to its ability to cause tumours following inhalation or alcohol consumption in animals. Humans are constantly exposed to AA through inhalation from the environment through cigarette smoke, vehicle fumes and industrial emissions as well as by persistent alcohol ingestion. Individuals with deficiencies in the enzymes that are involved in the metabolism of AA are more susceptible to its toxicity and constitute a vulnerable human population. Studies have shown that AA induces DNA damage and cytogenetic abnormalities. A study was undertaken to elucidate the clastogenic effects induced by AA and any preceding DNA damage that occurs in normal human lung fibroblasts as this will further validate the detrimental effects of inhalation exposure to AA. AA exposure induced DNA damage, involving DNA double strand breaks, which could possibly occur at the telomeric regions as well, resulting in a clastogenic effect and subsequent genomic instability, which contributed to the cell cycle arrest. The clastogenic effect induced by AA in human lung fibroblasts was evidenced by micronuclei induction and chromosomal aberrations, including those at the telomeric regions. Co-localisation between the DNA double strand breaks and telomeric regions was observed, suggesting possible induction of DNA double strand breaks due to AA exposure at the telomeric regions as a new mechanism beyond the clastogenic effect of AA. From the cell cycle profile following AA exposure, a G2/M phase arrest and a decrease in cell viability were also detected. Therefore, these effects due to AA exposure via inhalation may have implications in the development of carcinogenesis in humans.Inter-individual variations in DNA repair capacity (DRC) for repairing pesticide-induced DNA oxidation damage may influence adverse health outcomes. We aimed to evaluate whether polymorphisms in genes involved in nucleotide excision repair (NER) pathway could modulate DNA damage in pesticide-exposed agricultural workers. Xeroderma pigmentosum group F (XPF) (Arg415Gln, G1244A, rs1800067), xeroderma pigmentosum group G (XPG) (Asp1104His, G3507C, rs17655), excision repair cross complementation group 1 (ERCC1) (3'UTR, C8092A, rs3212986) and ERCC1 (Asn118Asn, C19007T, rs11615) polymorphisms were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique in 225 pesticide-exposed agricultural workers and 225 controls from Punjab, North-West India. The assessment of DNA damage was carried out by alkaline comet assay. Kruskal-Wallis test was used to evaluate the association of gene polymorphisms in NER pathway with DNA damage. Pesticide-exposed agricultural workers carrying variant XPF Gln/Gln (AA) genotype showed higher comet tail length (p less then 0.01) than wild type Arg/Arg (GG) genotype. The comet tail length (p less then 0.01) was found to be significantly increased in exposed agricultural workers carrying XPG His/His (CC) genotype than wild-type Asp/Asp (GG) genotype. In relation to the individuals carrying wild type ERCC1 3'UTR CC genotype, exposed individuals with variant ERCC1 3'UTR CA genotype showed elevation in the comet tail length (p = 0.029). However, we found no association of ERCC1 Asn118Asn (C19007T) genotype with DNA damage. These results indicate that XPF, XPG and ERCC1 genes of NER pathway may modulate the efficacy of the DNA repair system against pesticide exposure in our population.Ataxia-telangiectasia (AT) is a rare inherited recessive disorder which is caused by a mutated Ataxia-telangiectasia mutated (ATM) gene. Hallmarks include chromosomal instability, cancer predisposition and increased sensitivity to ionizing radiation. The ATM protein plays an important role in signaling of DNA double-strand breaks (DSB), thereby phosphorylating the histone H2A.X. Non-functional ATM protein leads to defects in DNA damage response, unresolved DSBs and genomic instability. The aim of this study was to evaluate chromosomal aberrations and γH2A.X foci as potential radiation sensitivity biomarkers in AT patients. For this purpose, lymphocytes of 8 AT patients and 10 healthy controls were irradiated and induced DNA damage and DNA repair capacity were detected by the accumulation of γH2A.X foci. The results were heterogeneous among AT patients. Evaluation revealed 2 AT patients with similar γH2A.X foci numbers as controls after 1 h while 3 patients showed a lower induction. In regard to DNA repair, 3 of 5 AT patients showed poor damage repair. Therefore, DNA damage induction and DNA repair as detected by H2A.X phosphorylation revealed individual differences, seems to depend on the underlying individual mutation and thus appears not well suited as a biomarker for radiation sensitivity. In addition, chromosomal aberrations were analyzed by mFISH. An increased frequency of spontaneous chromosomal breakage was characteristic for AT cells. After irradiation, significantly increased rates for non-exchange aberrations, translocations, complex aberrations and dicentric chromosomes were observed in AT patients compared to controls. The results of this study suggested, that complex aberrations and dicentric chromosomes might be a reliable biomarker for radiation sensitivity in AT patients, while non-exchange aberrations and translocations identified both, spontaneous and radiation-induced chromosomal instability.In a cross-sectional study of women in a nursing team at a university hospital in southern Brazil, we studied DNA damage, salivary cortisol levels, and cognition. DNA damage was measured in blood leukocytes with the comet assay and the micronucleus test. Salivary cortisol levels were determined upon waking, 30 min later, and at bedtime. Cognition was evaluated according to the Stroop, Digit span and Word span tests. Cortisol levels on waking up were associated negatively with the number of years the employee worked at the institution and positively with the DNA damage in comet assay. Cognitive scores were lower when the cortisol levels were low at awakening and high at bedtime; and were associated positively with educational level. Phorbol 12-myristate 13-acetate manufacturer Cortisol status may influence overall health as well as essential work skills, such as attention.Phorbol 12-myristate 13-acetate manufacturer