In addition, SF is very active against a large number of clinical isolates of H. pylori, including many strains that are resistant to conventional antibiotics such as clarithromycin and metronidazole. This immediately raises the question of whether dietary administration of SF may be a practical and economically viable treatment to combat H. pylori infection on a global scale.
Clinical case and mouse trials of H. pylori have shown that radicicic acid significantly reduces colonization and inflammation in H. pylori infections, although it does not completely cure them.
Although the enzyme urease was crystallized in 1926 from the bean, its molecular structure has only recently been elucidated.
Urease from plants and bacteria has a very high molecular weight (1.1 million daltons) and is a highly homologous molecule containing 12 thiol-rich catalytic subunits (12 cysteine residues per subunit) with two nickel ions (Ni2 +) in each active site.?
The reactivity of these cysteine thiols and their modification by reversible inhibitors and irreversible inactivators has been extensively studied and reported. Many cysteine residues are susceptible to the effects of inhibition by Michael reaction receptors (e.g., α,β-unsaturated ketones). It is therefore not surprising that isothiocyanates (e.g., SF) are effective inactivators of urease.
References:
[1] N. Ha, S. Oh, J.Y. Sung, K.A. Cha, M. Lee, B. Oh, Supramolecular assembly and acid resistance of Helicobacter pylori urease, Nature Structure Biol. 8 (6) (2001) 505-509.