Food and Chemical Toxicology, In Press, Accepted Manuscript
Honey, both unifloral (Syzygiumcumuni) and bifloral, demonstrated strong antimutagenicity against physical (UV, γ) and chemical (Ethylmethane sulfonate) mutagens as ascertained by rpoB/RifR and Ames tests.
The effect of honey was evaluated in radiation (UV or γ) exposed E. coli cells for SOS response, a well known error prone repair pathway known to significantly contribute to mutagenicity by quantifying LexA repressor level, measuring cell filamentation frequency, and prophage induction by SIVET (Selectable – In - Vivo Expression Technology) assay. LexA was almost completely degraded, phenotypically long filamentous cells (∼30 μm) were formed, and SIVET induction frequency was increased in radiation exposed E. coli cultures, however these changes were significantly inhibited in presence of honey confirming its strong antimutagenic nature. Further, rpoB/RifR mutation frequency upon UV exposure in E. coli recA- cells was found to be negligible, whereas, E. coliumuC- and umuD- knockouts showed comparatively higher mutation frequency. Honey did not show any effect on mutagenesis in these knockouts, indicating the SOS dependence of the observed mutagenesis.
Honey was also found to suppress EMS induced mutagenesis but through SOS independent mechanism.
Phenolics present in honey were found to be one of the important factors contributing to the antimutagenicity of honey.
Highlights
► Pollen analysis indicated commercial Indian honey as unifloral and bifloral.
► It showed broad spectrum antimutagenicity by Ames and E .colirpoB/RifR tests.
► Honey suppressed E. coli SOS response, an error-prone repair process.
► Error-prone repair is one of the major causes of mutagenesis.
► Honey inhibited LexA degradation, cell filamentation and prophage induction.
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