Evaluation of Bee Venom Induced Toxicity: Toxicity and Management

Authors : Sıdıka Genç, Kübra Karabulut, Esmanur Niğde, Şevval Büyükgöçmen, Ali Taghizadehghalehjoughi

Pages : 514-520

Doi:10.35229/jaes.1658697

View : 51 | Download : 64

Publication Date : 2025-07-31

Article Type : Research Paper

Abstract :Inflammation and increased cellular ROS levels caused by bee venom can increase formation of necrotic tissue and allergies. Many methods are used for bee venom induced toxicity. Two agents with therapeutic effects and pharmacological value have been included in these treatment options to decrease induced toxicity. L-tryptophan causes a decrease in the level of inflammation and the amount of ROS. Similarly, Amygdalin, which also targets the mTOR/AKT pathway and reduces inflammation, causes a decrease in FAK, ILK and β-catenin concentrations by inhibiting the expression of β1 and β4 integrins. Application of high doses of bee venom causes sensitization of nociceptors by activating TRPV1 via PLA2 cascade, which contains mellitin. This may result in pain and inflammation. We aimed to examine the toxic effects of bee venom by creating a wound model in the fibroblast cell line. After a linear wound was opened, the cells were exposed to bee venom (25 mg/ml) for 15 minutes. L-tryptophan and Vit B17 doses were applied at the end of 15 minutes. After 24 hours of incubation, wound healing was visualized and cell viability and oxidative damage tests were performed. The results showed that especially BV+ B17 + LT had a 60% effect on viability compared to the bee venom control group, resulting in wound closure. It was also determined that cellular ROS level decreased. All these results show that the combination of L-tryptophan and amygdalin has therapeutic efficacy on difficult-to-heal wounds.
Keywords : Arı Zehiri, Toksisite, L-Triptofan, B17, NO

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