Protective role of melatonin in ochratoxin a toxicity in rat heart and lung

Ochratoxin A (OTA) is a mycotoxin produced by different fungi. The most pronounced adverse effect of OTA is hepatonephrotoxicity. Melatonin (MEL) has an antioxidant effect and has free-radical scavenger properties. The effects of OTA on heart and lung tissue and possible ameliorating effects of MEL were investigated in rats. Twenty-four rats were allocated to three groups (each with eight rats): control; OTA-treated group (OTA dose 289 microg kg(-1) per day); and OTA + MEL-treated group (MEL dose 10 mg kg(-1) per day). After 30 days of treatment, the histopathological changes in the heart and lung of all groups were examined. Compared with the control rats, myocardial tissue of rats treated with OTA showed extensive cytoplasmic vacuole formation, necrosis of the myocytes, dissolution of the nucleus, clumped fibres, fibrillolysis, swollen myocardial fibres, small haemorrhagic areas and hyperaemic vessels (P <0.05). In addition, lungs of rats treated with OTA showed alveolar congestion, alveolar cell hyperplasia, prominent alveolar septal vessels, variable intensity loss of alveolar architecture, intraparenchymal inflammatory infiltration, intraparenchymal hyperaemic vessels, respiratory epithelial proliferation, perivascular and peribronchial inflammation, pneumonic infiltration, distorted appearance of lung parenchyma and emphysematous areas (P <0.05). In comparison with the OTA groups, the ameliorating effects of MEL in the lung damage parameters were on alveolar cell hyperplasia, prominent alveolar septal vessels, variable intensity loss of alveolar architecture, intraparenchymal inflammatory infiltration, perivascular inflammatory inflammation, distorted appearance of lung parenchyma and focal emphysematous areas in lung (P <0.05). Melatonin also significantly reduced myocardial damage in most of the parameters: extensive cytoplasmic vacuole formation, necrosis of the myocytes, clumped fibres, fibrillolysis, small haemorrhagic areas and hypaeremic vessels in heart (P <0.05). On the other hand, MEL did not lower the degree of damage in lung and heart to the level of the control rats, except for the parameters of the interstitial oedema and small haemorrhagic areas only in myocardial tissue. Histopathological findings showed that OTA induced damage in heart and lung and MEL treatment significantly reduced the degree of damage.