Abstract
Cigarette smoke (CS) and ethanol (EtOH) are known to synergize in the causation of cancers of the upper aerodigestive tract and of the liver. Little is known about possible interactions between these agents in other organs. These premises prompted us to evaluate the clastogenic effects resulting from the inhalation for 3 weeks of mainstream CS and oral administration of EtOH, which were tested either individually or in combination in cells of adult BDF1 mice and their fetuses. CS exerted clastogenic effects in haematopoietic cells of adult male mice by increasing the frequency of micronucleated erythroid cells both in bone marrow and in peripheral blood as well as the frequency of micronucleated and polynucleated pulmonary alveolar macrophages. Likewise, exposure to CS of pregnant mice resulted in a clastogenic damage in maternal bone marrow cells and in the liver and peripheral blood of their fetuses. Under all experimental conditions, EtOH was consistently devoid of clastogenic effects when given alone. In adult mice, EtOH exhibited a mild stimulating effect on the clastogenicity of CS in haematopoietic cells, while an opposite effect was observed in the respiratory tract, where EtOH attenuated the cytogenetic alterations induced by CS in pulmonary alveolar macrophages. At variance with the mild synergism observed in haematopoietic cells of adult mice, EtOH inhibited the clastogenicity of CS in the liver and peripheral blood cells of transplacentally exposed fetuses. Therefore, the effects of EtOH in CS-exposed mice show different trends depending both on the life stage and on the cells analyzed.
Highlights
Cigarette smoke (CS) and ethanol (EtOH) are two major risk factors for cancer and for a variety of other chronic degenerative diseases
EtOH is a single chemical compound that exerts its toxicity via its metabolite acetaldehyde, which is generated by cytoplasmic alcohol dehydrogenase, and reactive oxygen species (ROS), which are predominantly generated by the microsomal cytochrome P450 2E1 (CYP2E1)
At the end of that period, increases in the frequencies of both MN polychromatic erythrocytes (PCE) in bone marrow and of MN and PN pulmonary alveolar macrophages (PAM) in the lower respiratory tract were observed in mainstream CS (MCS)-exposed mice
Summary
Cigarette smoke (CS) and ethanol (EtOH) are two major risk factors for cancer and for a variety of other chronic degenerative diseases. Smoking in humans has been associated with cancers targeting a number of tissues in the respiratory system, including the nasal cavity and paranasal sinuses, pharynx Interactions between Ethanol and Cigarette Smoke oropharynx and hypopharynx), larynx, and above all trachea and lung, as well as in the urinary tract (kidney pelvis, ureter, and bladder), digestive system (oral cavity, oesophagus, stomach, colon-rectum, liver, and pancreas), reproductive tract (ovary and uterine cervix), and hematopoietic system (myeloid leukemia) [4]. Like CS, EtOH is classified as a human carcinogen, but its targets are limited to the proximal aerodigestive tract (oral cavity, pharynx, larynx), to the digestive tract (oesophagus, liver, colorectum) and to female breast [8]
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