Effects of Escherichia coli strain Nissle 1917 on arsenic-challenged goldfish (Carassius auratus): histological evidence

Arsenic (As) contamination in natural water resources has become a great disaster throughout the world posing serious health problems. The current study was performed to evaluate the protective effects of Escherichia coli strain Nissle 1917 (EcN) against As exposure in goldfish (Carassius auratus). Fish were fed three times a day with 4.00% of body weight of diet with different doses (0.00, 1.00 x 106, 1.00 x 107 and 1.00 x 108 CFU g-1) of EcN for 80 days and then, challenged with 20.00 mg L-1 As for 96 hr under stagnant flow. Physicochemical characteristics of the inlet water were temperature of 25.10 & PLUSMN; 0.70 C, pH of 7.30 & PLUSMN; 0.20 and dissolved oxygen of 7.30 & PLUSMN; 0.30 mg L-1 and 50.00% of water was exchanged once a week. Afterwards, fish were euthanized with a clove oil solution (50.00 & mu;L L-1) and tissues were dissected from each fish and immediately fixed in 10.00% buffered formalin. The histopathological results indicated that the supplemented EcN did not have any side effects on various organs. It was also observed that the damages to kidney, liver, gill and skin were pronounced in fish exposed to As. However, the histopathological damages induced by As in fish tissues were less pronounced in the EcN-treated groups compared to the fish fed with the basal diet. Lamellar blood congestion in gills and epidermal cells detachment from the skin surface as well as hepatocytes, enterocytes and tubular necrosis were reduced in treated groups. These findings indicate that EcN has the potential to ameliorate the As induced organ toxicity.& COPY; 2023 Urmia University. All rights reserved.

Automated summary

This study evaluated the protective effects of Escherichia coli strain Nissle 1917 (EcN) against arsenic (As) exposure in goldfish. The results showed that the supplemented EcN could mitigate the damages caused by As to the organs of fish, indicating its potential to alleviate organ toxicity.