Menthol exposure induces reversible cardiac depression and reduces lipid peroxidation in the heart tissue of tambaqui Colossoma macropomum

2021 
Abstract Exposure to menthol is expected to alleviate physiological and oxidative stress in fish. Yet, its effects as an anesthetic-like compound on the heart function and associated physiological and biochemical changes still need further clarification. This study aimed to analyze the effects of menthol on the cardiac function and oxidative stress responses of Colossoma macropomum exposed to short-term baths. Fish were divided into three groups: control, menthol-exposed fish (40, 60 and 80 mg L−1) and fish in recovery. The electrocardiogram (ECG) tracing patterns, wave intervals (RR; QT), complex duration (QRS) and heart rate were assessed after 5 min recordings throughout exposure and recovery. Total antioxidant capacity against peroxyl radicals (ACAP), glutathione S-transferase (GST) activity and lipoperoxidation (LPO) levels were also evaluated in the heart tissue. All concentrations of menthol depressed the heart rate and prolonged RR and QT intervals in a concentration-dependent fashion. QRS complex duration was only reduced at the highest dose of menthol. During recovery, heart rate and mean amplitude were still reduced at 60 or 80 mg L−1 menthol, whereas wave intervals were still longer at these concentrations. Notwithstanding, QRS complex resumed its normal duration during recovery. GST activity and ACAP were unchanged in fish exposed to menthol. However, LPO reduced in fish exposed to 40 and 60 mg L−1 menthol. In conclusion, all concentrations of menthol induced anesthesia in C. macropomum without causing mortality, albeit provoking transient cardiac alterations. Menthol at 40 and 60 mg L−1 could be considered suitable concentrations to immobilize fish as they not only did not compromise cardiac function but reduced LPO in the heart. Yet, menthol at 80 mg L−1 or higher doses should be avoided as there is a potential for the emergence of a life-threatening cardiac depression and oxidative stress.
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