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Year : 2018  |  Volume : 13  |  Issue : 2  |  Page : 89-98

Inhibitory effect of bee venom against potassium bromate causing genetic toxicity and biochemical alterations in mice

Department of Cell Biology, National Research Centre, Dokki, Giza, Egypt

Correspondence Address:
Dr. Abeer H Abd El-Rahim
Department of Cell Biology, National Research Centre, Dokki, Giza 12922
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/jasmr.jasmr_24_18

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Background/aim Bee venom (BV) therapy is a highly effective treatment, capable of improving one’s health. The present study attempts to assess the effect of BV on the toxicity of oral administration of potassium bromate (KBrO3) which has been widely used in food and cosmetic industries. Materials and methods Sixty adult male mice were gavaged with KBrO3 at two doses (100 and 200 mg/kg body weight) for 10 days. Afterwards, BV at a dose of 120 μg/kg body weight was injected subcutaneously three times per week for two successive weeks. The genetic study was performed using chromosomal aberration and micronucleus formation in the bone marrow, DNA fragmentation in liver cells and by sperm analysis. In addition, serum biochemical markers such as catalase and malondialdehyde, kidney, and liver functions were assessed. Results The results have shown that KBrO3 caused DNA damage that represented the increase in the frequencies of chromosome abnormalities, micronuclei formation, percentage of DNA fragmentation, and sperm morphological abnormalities. Meanwhile, the results showed that KBrO3 exhibited severe toxicity for antioxidant activities for liver and kidney functions. Conversely, BV significantly decreased the frequencies of DNA damage in all aforementioned parameters induced by KBrO3. In addition, it improved the antioxidant activities and the function of the liver and kidneys. Conclusion BV has a potent ameliorating effect against the KBrO3 hazard impacts in animal tissues especially at higher doses. This observation indicated that BV could be a potential therapeutic agent in the treatment of KBrO3 risk.

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