Royal jelly (RJ) is widely used as a food supplement for anti-aging and beauty. However, its use has been linked to asthma and hemorrhagic colitis. Since its mechanisms of toxicity have not been fully identified, we conducted an investigation to elucidate its molecular and cytogenetic effects. Using human lymphocytes in vitro, treatments with RJ (0.0005-5 mg/ml) for 3 h did not induce sister chromatid exchanges until 5 mg/ml was used. Treatments for 24 h showed a dose-dependent reduction in BCL2/BAX, c-MYC/BAX and HO-1/BAX ratios. The exception was the NRF2/BAX ratio, showing a dose-dependent reduction at low doses, but a marked increase at the highest dose. The hTERT/BAX ratio was maintained at approximately a 1.2-fold increase but decreased to nearly normal at the highest dose. Our findings indicated that the lowest dose of RJ treatment provided maximum benefits, mainly through hTERT activation relating to prolonged lifespan. The highest dose of RJ inhibited cell survival, cell proliferation and an antioxidative enzyme; nevertheless, it still activated an antioxidative response through NRF2 and maintained telomeres during cell crisis. RJ treatment at 0.05 mg/ml increased cyclin E, BCL2 and BAX to maximum levels indicating that throughout the active cell cycle, both cell survival and cell apoptosis increased. Using the gene expression ratios over BAX, similar to BCL2/BAX, provided more informative data than using individual protein levels alone. With these informative ratios, our results confirm the potential benefits of RJ in enhancing lifespan and activation antioxidative power. Further, in vivo mechanistic studies will be useful in validating these results.

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Genoprotective effects of royal jelly (RJ) treatments against doxorubicin (DXR), a potent genotoxic chemotherapeutic compound in human lymphocytes were investigated using the sister chromatid exchange (SCE) assay, and their molecular mechanisms were examined by Western blot. Results showed that RJ pretreatments at 0.005 and 0.05 mg/mL significantly decreased DXR-induced SCE levels by 1.2-fold (p<0.05), compared to DXR treatment alone. Co-treatment of RJ (5 mg/mL) with DXR (0.2 µg/mL) increased the ratios of BCL2/BAX (1.5-fold), NRF2/BAX (1.3-fold), and hTERT/BAX (1.1-fold) compared to the DXR alone, suggesting its power in enhancing cell survival, antioxidative potentials, and longevity over cell death. The study suggested that RJ protected human cells from DXR-induced genotoxicity, possibly mediated through anti-apoptotic, anti-oxidative, and anti-aging properties of RJ. However, lower doses of RJ co-treatments enhanced DXR toxicity. Further, in vivo molecular study is required to validate this in vitro study.

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