Tea tree oil attenuates cerebral damage in silver catfish (Rhamdia quelen) fed with an aflatoxin-contaminated diet

Abstract

Aflatoxins are fungal metabolites that contaminate foods and feeds, causing adverse health effects in humans and animals. From an economic standpoint, aflatoxins represent one of the most severe problems for the livestock and feed industries. Currently, natural supplements are used to prevent various fungal infections in farmed fish. The aim of the present study was to determine whether dietary supplementation with tea tree oil (TTO: Melaleuca alternifolia) would prevent or minimize the effects of aflatoxin (AFB) on silver catfish (Rhamdia quelen). Four treatments were tested: control (without AFB);AFB (fish fed with a mycotoxin-contaminated diet – 1893 μg/kg of AFB1 and 52.2 μg/ kg AFB2); TTO (fish fed with a control diet +1 mL/kg of TTO), and TTO + AFB (fish fed with a mycotoxin contaminated diet - 2324 μg/kg of AFB1 and 43.5 μg/kg AFB2 + 1 mL/kg of TTO). Treatments were tested in three replications and were analyzed at days 5 and 10 of dietary intake. Increased activities of nucleoside triphosphate diphosphohydrolase (NTPDase) using ADP as substrate and adenosine deaminase (ADA) were observed after 5 day-feeding with AFB1 diet. Feed contaminated with AFB1 caused an inhibition of acetylcholinesterase (AChE) activity. Aflatoxicosis caused severe gliosis and subarachnoid edema. The addition of TTO in AFB1-contaminated feed prevented the inhibition of AChE activity and increased ADA activity. TTO supplementation increased p2y11 receptor expression, most likely in an attempt to deal with inflammation caused by aflatoxicosis. TTO treatment ameliorated aflatoxin-associated brain tissue damage. These findings suggest that TTO supplementation reduces the effects of aflatoxicosis in silver catfish brain tissue because it prevents most changes caused by AFB1-contaminated diet. Overall, the results obtained in the present study suggest that TTO could be used as an aflatoxin-detoxifying agent in fish.