The Venom of Tarantula Cubensis (Theranekron) Reduces Apoptosis and Mitochondrial Oxidative Toxicity Caused by NaIO3–Induced Age-Related Macular Degeneration in Human Retinal Pigment Epithelium Cells

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ARGUN M., ÇELİK Ö.

Journal of Cellular Neuroscience and Oxidative Stress, cilt.18, sa.2, ss.1328-1335, 2026 (Scopus)

Özet

Excessive generations of apoptosis and oxygen free radicals (OFRs) are two main common reasons of age-related macular degeneration (AMD). A homeopathic preparation of the Tarantula Cubensis spider venom is Theranekron (TNE). The antiapoptotic and antioxidant actions of TNE were indicated in different disease models except AMD. We investigated the protective actions of the TNE and TRPM2 antagonist (N-(p-amylcinnamoyl) anthranilic acid, ACA) on AMD (sodium iodate [NaIO3])mediated apoptosis and oxidative toxicity in ARPE-19 cells. The ARPE-19 cells were incubated for 24 h in five primary groups: control, 108 ug/mL TNE, 10 mM NaIO3, NaIO3 + TNE, and NaIO3 + 25 uM ACA (last one hour of NaIO3 incubation). The NaIO3 treatment increased markers of apoptosis (caspase-3, caspase-8, and caspase-9) and oxidative stress (OFRs and mitochondrial membrane dysfunction), while diminishing cell viability. The treatments of TNE and ACA decreased the NaIO3-induced increases of apoptotic and oxidant markers, although the treatments increased cell viability. In conclusion, TNE and ACA treatments reduced NaIO3-caused oxidative degeneration and apoptosis in the ARPE-19 cells. TNE through TRPM2 inhibition is a possible treatment for AMD-induced apoptosis and OFR production.