Polyphenols are an important functional minor component of virgin olive oils that are responsible for the key sensory characteristics of bitterness, pungency, and astringency. Polyphenols were isolated from virgin olive oils by using liquid/liquid extraction and then separated by using reverse phase HPLC followed by fraction collection. The sensory qualities of the isolated polyphenols were evaluated, and almost all fractions containing polyphenols were described as bitter and astringent. However, the fraction containing deacetoxy-ligstroside aglycon produced a strong burning pungent sensation at the back of the throat. In contrast, the fraction containing the analogous deacetoxy-oleuropein aglycon, at an equivalent concentration, produced only a slight burning/numbing sensation, which was perceived more on the tongue. No other polyphenol fractions from the analyzed oils produced the intense burning sensation; thus, deacetoxy-ligstroside aglycon is the polyphenol responsible for the majority of the burning pungent sensation found in pungent extra virgin olive oils.

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Seafood frequently contains high concentrations of arsenic (approximately 10-100 mg/kg dry weight). In marine algae (seaweed), this arsenic occurs predominantly as ribose derivatives known collectively as arsenosugars. Although it is clear that arsenosugars are not acutely toxic, there is a possibility of arsenosugars having slight chronic toxicity. In general, trivalent arsenicals are more toxic than their pentavalent counterparts, so in this work we examine the hypothesis that trivalent arsenosugars might be significantly more toxic than pentavalent arsenosugars in vitro. We compared the in vitro toxicity of (R)-2,3-dihydroxypropyl-5-deoxy-5-dimethylarsinoyl-beta-D-riboside, a pentavalent arsenosugar, to that of its trivalent counterpart, (R)-2,3-dihydroxypropyl-5-deoxy-5-dimethylarsino-beta-D-riboside. The trivalent arsenosugar nicked plasmid DNA, whereas the pentavalent arsenosugar did not. The trivalent arsenosugar was more cytotoxic (IC50 = 200 microM, 48 h exposure) than its pentavalent counterpart (IC50 > 6000 microM, 48 h exposure) in normal human epidermal keratinocytes in vitro as determined via the neutral red uptake assay. However, both the trivalent and the pentavalent arsenosugars were significantly less toxic than MMA(III), DMA(III), and arsenate. Neither the pentavalent arsenosugar nor the trivalent arsenosugar were mutagenic in Salmonella TA104. The trivalent arsenosugar was readily formed by reaction of the pentavalent arsenosugar with thiol compounds, including, cysteine, glutathione, and dithioerythritol. This work suggests that the reduction of pentavalent arsenosugars to trivalent arsenosugars in biology might have environmental consequences, especially because seaweed consumption is a significant environmental source for human exposure to arsenicals.

The mechanism of arsenic carcinogenesis is unclear. A complicating factor receiving increasing attention is that arsenic is biomethylated to form various metabolites. Eleven different arsenicals were studied for in vitro genotoxicity to supercoiled DNA (pBR 322 and phiX174). Five arsenicals showed various degrees of positivity-monomethylarsonous acid, dimethylarsinous acid, monomethylarsine, dimethylarsine, and trimethylarsine. Supercoiled DNA, blotted on nitrocellulose filter paper, was exposed to gaseous arsines by suspending the filter paper above aqueous reaction mixtures of sodium borohydride and an appropriate arsenical. All three methylated arsines damaged DNA; inorganic arsine did not. Arsines were generated in situ in reaction mixtures containing DNA by reaction of sodium borohydride with arsenite, monomethylarsonous acid, dimethylarsinous acid, and trimethylarsine oxide, at pH 8.0. Both dimethylarsine and trimethylarsine (generated from 200 micro M dimethylarsinous acid and trimethylarsine oxide, respectively) damaged DNA in less than 30 min. Under certain conditions, the two most potent genotoxic arsines, trimethylarsine and dimethylarsine, are about 100 times more potent than dimethylarsinous acid (the most potent genotoxic arsenical previously known). There was no evidence to suggest that anything other than the arsines caused the DNA damage. Possible models for the biological production of arsines were examined. The coenzymes, NADH and NADPH, are biological hydride donors. When NADH or NADPH (5 mM) were incubated with dimethylarsinous acid (0-2 mM) for 2 h, DNA damage was increased by at least 10-fold. A possible explanation for this result is that these compounds react with dimethylarsinous acid to generate dimethylarsine. DNA was incubated with a dithiol compound, dithioerythritol (5 mM), and trimethylarsine oxide (0.5 mM) for 2 h, and the reduction of trimethylarsine oxide to trimethylarsine resulted in DNA damage.