CHRONIC DOSE OF ATRAZINE INDUCES ELECTRICAL CARDIAC DISTURBANCES WITHOUT STRUCTURAL DAMAGE OR CONTRACTILE IMPAIRMENT IN MALE WISTAR RATS

Atrazine (ATR) is an herbicide used to control weeds in crops and a non-selective agent used to control vegetation in industrial areas. ATR can accumulate in soil and organs like gonads and liver, it was also reported as neurotoxic agent and pollutant. Knowledge regarding cardiotoxic effects of ATR remains limited, special regarding these effects in low chronic doses allowed. In that sense, we orally administrated ATR for 28 days in male rats with maximum acceptable daily intake (ADI) of 0,02 mg/kg/day. Our findings demonstrated ATR altered excitability of in vivo e ex vivo hearts on ECG. For in vivo, ATR preserved waves duration, except for a lower QRS complex duration (CTR 42.52 ± 2.46 vs. ATR 39.65 ± 1.47, p = 0.02). In ex vivo experiment, higher susceptibility to arrhythmic events after reperfusion (CTR 9.4 ± 4.1 vs. ATR 16.17 ± 5.19, p = 0.04). Electrophysiology property of isolated cardiomyocytes showed increase in maximal velocity AP depolarization in ATR group (CTR 153.0 ± 49.99 vs. ATR 201.20 ± 57.72, p = 0.047). In relation to echocardiogram, ATR was able to promote aortic (CTR 0.88 ± 0.02 vs. ATR 0.84 ± 0.02, p = 0.03) and pulmonary flow changes (CTR 0.63 ± 0.03 vs. ATR 0.66 ± 0.02, p = 0.06), also an increase in E/A ratio (CTR 1.13 ± 0.06 vs. ATR 1.85 ± 0.15, p = 0.0001). Histological parameters showed no tissue changes or abnormalities, and heart slice follow reperfusion didn’t showed infarcted area (CTR 32.20 ± 9.51 vs. ATR 33.94 ± 6.74, p = 0.72). Contractile function remains unchanged, correlates with preserved calcium dynamics. Overall, ATR at allowed ADI concentration showed impact in heart function. A plausible mechanistic explanation for these findings is that ATR enhances oxidative stress during reperfusion, thereby promoting redox-dependent electrical remodeling.