Background Presence of chromosome damage in lymphocytes of patients affected by several diseases, including cancer, was detected by the micronucleus (MN) assay. Individual susceptibility to DNA damage, considered as a risk factor for cancer, can be also evaluated using the bleomycin (BLM) sensitivity test. Materials and methods We aimed to evaluate spontaneous or BLM-induced MN frequencies in autoimmune (AI, n = 19) and non autoimmune (NAI, n = 11) thyroid patients, not receiving 131I radiometabolic therapy with respect to a control group of 18 healthy subjects. According to thyroid function, patients were also divided into hypothyroid (n = 10), euthyroid (n = 13) or hyperthyroid (n = 7) subjects. Results Spontaneous MN frequencies of AI and NAI patients did not differ from those of controls. Hypothyroid patients had more elevated MN basal levels (9·00 ± 1·71‰) than hyperthyroid (3·75 ± 1·17‰, P < 0·05) and euthyroid (5·38 ± 0·97‰, P < 0·01) patients or healthy subjects (4·17 ± 0·63‰, P < 0·01). In particular, the hypothyroid AI group showed the highest value (9·79 ± 2·26‰, P < 0·01). All thyroid patients responded differently to BLM than controls (39·90 ± 2·48‰ vs. 31·08 ± 2·51‰, P = 0·0377). The NAI group had BLM-induced MN levels (45·00 ± 2·56‰) significantly higher (P = 0·0215) than AI patients (36·95 ± 3·49‰) or healthy subjects (31·08 ± 2·51‰). No significant difference was seen when patients were stratified according to autoimmunity. Conclusions We report that hypothyroid patients exhibit a moderate increase in the level of spontaneous genome damage, and that AI thyroid patients resulted to be less sensitive than NAI patients to the mutagen sensitivity test. In prospective, it may be of interest to reinvestigate hypothyroid patients when correction of their dysfunction is achieved.
|Autori interni:||SCARPATO, ROBERTO|
|Autori:||SCARPATO R; TUSA I; ANTONELLI A; FALLHAI P; SBRANA I|
|Titolo:||Spontaneous and bleomycin-induced chromosome damage in non cancer thyroid patients|
|Anno del prodotto:||2009|
|Digital Object Identifier (DOI):||10.1111/j.1365-2362.2009.02214.x|
|Appare nelle tipologie:||1.1 Articolo in rivista|