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Biomedical subjects

M Artuso

Publications and source records attributed to M Artuso.

At least 19 recordsLinked to original sources
PubMed1996

The role of Ataxia telangiectasia and the DNA-dependent protein kinase in the p53-mediated cellular response to ionising radiation.

The DNA-dependent protein kinase (DNA-PK), whose catalytic subunit shows structural similarities to the Ataxia telangiectasia (AT) gene product (ATM), has also been implicated in the p53-mediated signal transduction pathway that activates the cellular response to DNA damage produced by ionizing radiation. DNA-PK activity however was not found to be related to the transcriptional induction of WAFl/CIP1(p2l) in AT lymphoblastoid cell lines, following treatment with ionizing radiation. Normal protein and transcription levels of Ku70 and Ku80, as well as DNA-PK activity, were found in six different AT cell lines, 1-4 h following exposure to ionizing radiation, timepoints where reduced and delayed transcriptional induction of WAF1/CIP1 (p21) was observed. WAF1/CIP1 (p21) was found to be transcriptionally induced by p53 in normal cell lines over this same time period following exposure to ionizing radiation. These results suggest that despite the findings that in vitro DNA-PK may phosphorylate p53, in vivo it would not appear to play a central role in the activation of p53 as a transcription factor nor can it substitute for the ATM gene product in the cellular response following exposure to ionizing radiation.

Animals↗
PubMed1996

Aflatoxin exposure and cytogenetic alterations in individuals from the Gambia, West Africa.

Aflatoxin-albumin adducts in peripheral blood provide a measure of exposure to aflatoxin over the previous 2-3 months. In the present study, the levels of these adducts were determined in a group of individuals from The Gambia, West Africa and were compared in a cross-sectional study to the levels of various cytogenetic alterations (chromosomal aberrations, micronuclei, sister chromatid exchanges) in the same individuals to test whether an increase in genetic damage is associated with an increased exposure in this population. Of 35 subjects tested for aflatoxin-albumin adducts, all but 3 were positive. There were no correlations between the adduct level and the number of cytogenetic abnormalities at the individual level. A comparison of the cytogenetic alterations was made between Gambian individuals and a group of 22 healthy people from Italy where aflatoxin exposure is expected to be low. The levels of structural chromosomal aberrations, sister chromatid exchanges and micronuclei were all higher in the former group. Overall, these data are indicative of a higher exposure to genotoxins in Gambian subjects, one of which are aflatoxins, but suggest that more specific genetic markers of aflatoxin exposure are required to further examine the link between aflatoxin exposure and genetic alterations.

Adolescent↗
PubMed1996

Molecular epidemiology of skin cancers: DNA repair and non-melanocytic skin cancer.

Exposure to sunlight has been clearly associated with non-melanocytic skin cancer, however individual susceptibility differs considerably. Ethnic origin and pigmentary characteristics are generally accepted as risk factors. Another important defense mechanism is the ability to repair DNA photoproducts. In the inherited disorder xeroderma pigmentosum the inability to repair such DNA damage, associated with a high incidence of skin cancers, suggests an important role for DNA repair capacity in the etiology of this cancer. The development of an in vitro repair assay based on human peripheral blood lymphocytes, has allowed the evaluation of DNA repair capacity as a risk factor in population based studies. This article reviews recent developments in this field.

Animals↗
PubMed1995

The role of the Ataxia telangiectasia gene in the p53, WAF1/CIP1(p21)- and GADD45-mediated response to DNA damage produced by ionising radiation.

The inducible response of the tumour suppressor gene p53 has been examined following exposure to DNA-damaging agents in Ataxia telangiectasia (AT) cell lines, an autosomal recessive disorder with multiple clinical and biological abnormalities including sensitivity to ionising radiation. The p53 induction was significantly delayed and reduced in the 8 AT cell lines examined over the 6 h following irradiation with no dose response in p53 induction being observed compared to control cells. The increase of WAF1/CIP1(p21) and GADD45 mRNA, two genes transcriptionally activated by p53, was also reduced in the AT cell lines after such treatment. In contrast, the increase in p53 protein, WAF1/CIP1(p21) and GADD45 mRNA expression following exposure to the alkylating agent methylmethane sulphonate (25 and 100 micrograms ml-1) was similar in both cell types. No alterations in the expression of EBNA-5, an EBV-encoded nuclear antigen which has been shown to bind p53 or mutations in the p53 gene (exons 4 to 8) were found in the AT cell lines studied. The AT gene product would thus appear to be involved upstream of p53, GADD45 and WAF1/CIP1 (p21) in the signalling of the presence of strand breaks produced by ionising radiation, with this defect in response contributing to the high cancer risk and radiosensitivity observed in this disorder.

Alkylating Agents↗
PubMed1995

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Journal Article↗
PubMed1995

Cytogenetic biomonitoring of styrene-exposed plastic boat builders.

Earlier studies have produced evidence for an association between work-related styrene exposure and cytogenetic damage, while more recent studies have failed to show such an association. In the present study, chromosome aberrations (CA) and sister chromatid exchanges (SCE) were measured in peripheral blood lymphocytes of 46 male workers employed in a fiber-reinforced plastic boat building factory and exposed to styrene. Two groups of 23 workers each, characterized by different exposure levels (ranges: 2-120 mg/m3 and 86-1389 mg/m3 ambient air) were studied, fifty-one controls matched by sex, age and smoking habits were included. Randomized blood samples were analyzed for cytogenetic damage separately in two laboratories. Interlaboratory differences in the scoring of CA and SCE were noted. However, increases of the considered cytogenetic endpoints in exposed vs control groups were consistently observed in both laboratories. Multivariate statistical analysis of pooled data revealed increases of CA ranging between 19% (RR = 1.19; 95% C.I., 0.80-1.78; chromatid-type aberrations, low exposure group) and 144% (RR = 2.44; 95% C.I., 1.26-4.70; chromosome-type aberrations, high exposure group). Parallel excess of SCE in styrene exposed workers was also observed, although at a lesser extent (RR = 1.22; 95% C.I., 1.05-1.43, low exposure group; RR = 1.26; 95% C.I., 1.07-1.47, high exposure group). These findings suggest the presence of a causal association between occupational exposure to styrene and cytogenetic damage in the plastic boat building factory that was the object of the study.

Adult↗