Interactions of PLA2-s from Vipera lebetina, Vipera berus berus and Naja naja oxiana Venom with Platelets, Bacterial and Cancer Cells

Toxins

Mari Samel¹  Heiki Vija¹  Imbi Kurvet¹  Kai Künnis-Beres¹  Katrin Trummal¹  Juhan Subbi¹  Anne Kahru¹ 

[1] National Institute of Chemical Physics and Biophysics, Tallinn 12618, Estonia;

关键词: Snake venom;    Vipera lebetina;    Vipera berus berus;    Naja naja oxiana;    phospholipase A₂;    human platelet aggregation inhibition;    antibacterial;    bioluminescent bacteria;    cancer cells;   

DOI  :  10.3390/toxins5020203

来源: mdpi

【 摘 要 】

Secretory phospholipasesA₂ (sPLA₂s) form a large family of structurally related enzymes widespread in nature. Herein, we studied the inhibitory effects of sPLA₂s from Vipera lebetina (VLPLA₂), Vipera berus berus (VBBPLA₂), and Naja naja oxiana (NNOPLA₂) venoms on (i) human platelets, (ii) four different bacterial strains (gram-negative Escherichia coli and Vibrio fischeri; gram-positive Staphylococcus aureus and Bacillus subtilis) and (iii) five types of cancer cells (PC-3, LNCaP, MCF-7, K-562 and B16-F10) in vitro. sPLA₂s inhibited collagen-induced platelet aggregation: VBBPLA₂ IC₅₀ = 0.054, VLPLA₂ IC₅₀ = 0.072, NNOPLA₂ IC₅₀ = 0.814 μM. p-Bromophenacylbromide-inhibited sPLA₂ had no inhibitory action on platelets. 36.17 μM VBBPLA₂ completely inhibited the growth of gram-positive Bacillus subtilis whereas no growth inhibition was observed towards gram-negative Escherichia coli. The inhibitory action of sPLA₂s (~0.7 μM and ~7 μM) towards cancer cells depended on both venom and cell type. VBBPLA₂ (7.2 μM) inhibited significantly the viability of K-562 cells and the cell death appeared apoptotic. The sPLA₂s exhibited no inhibitory effect towards LNCaP cells and some effect (8%–20%) towards other cells. Thus, already sub-μM concentrations of sPLA₂s inhibited collagen-induced platelet aggregation and from the current suite of studied svPLA₂s and test cells, VBBPLA₂ was the most growth inhibitory towards Bacillus subtilis and K-562 cells.

【 授权许可】

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