Ethanol (ETOH) is commonly used as a drug solvent in experimental treatments of research animals, frequently without adequate controls to dissect out the effects of ETOH. We have explored the effects of ETOH administered to adult male Wistar rats in the drinking water (1% ETOH; 8 days). Controls rats were identically housed and given regular tap water. We have explored: a) the general status of the animals (red and white blood cells and platelets, blood glucose and protein levels); b) the catecholamine levels in renal artery, superior cervical ganglion and carotid body; in the last tissue we also studied catecholamine synthesis and release), and; c) the general redox status of the animals (glutathione potential and lipid peroxides in lung, liver and diaphragm and antioxidant power of plasma (PAP). We also monitored angiotensin-converting enzyme (ACE). Animals were humanely killed at the end of the experiment. Statistical significance was evaluated by unpaired t test. There were not differences between groups in body weight gain or in the amount of water drunk. ETOH ingested by experimental animals amounted to 0.27 ml/rat/day. Red cell count, haemoglobin, hematocrit leucocytes and platelets were not statistically different in both groups. Proteins levels were identical in both groups, but glucose (142.6 ± 8.43 mg/100ml) increased in the ETOH group to 251.0 ± 28.45; n =10). Norepinephrine levels in renal artery and superior cervical ganglion of control animals were, respectively, 11.64 ± 1.10 and 175.60 ± 11.26 pmol/mg tissue and decreased in the ETOH group to 7.20 ± 0.58 and 114.10 ± 9.47 pmol/mg tissue (n = 11-16; p < 0.001 in both cases). In the carotid body norepinephrine and dopamine levels were not different between groups, but the rate of synthesis and release of dopamine increased significantly in the ETOH group. The glutathione redox potential in diaphragm (-184.0 ± 2.05 mV) and liver (-223.3 ± 0.82 mV), but not in lung, rose in ETOH group to -190.9 ± 1.07 and -232.4 ± 2.75 mV, respectively, and lipid peroxides levels decreased in the same tissues. The PAP in control animals was equivalent to 1,349 ± 163.6 mM FeSO4 and in the ETOH rose to 2,036 ± 196.7 mM (n 13-16; p=0.011). ACE (332.8 ± 20.43 U/l) was significantly lower in ETOH group 187.3 ± 9.63 U/l; n = 10; p < 0.001). This wide range of effects of low doses of ETOH advise the use of adequate controls in studies that use this agent as solvent. Additionally, the data indicate that moderate doses of ETOH might protect against oxidant damage at the cost of producing marked hyperglycaemia.