Resorcinol 50% in Glycerol

In vitro and in vivo studies have demonstrated that resorcinol can inhibit peroxidases in the thyroid and subsequently block the synthesis of thyroid hormones and cause goiter [F61][L2747]. Resorcinol interferes with the iodination of tyrosine and the oxidation of iodide [F61][L2747]. In an in vitro study involving lactoperoxidase (LPO) and thyroid peroxidase (TPO), it was shown that the mechanism of these two enzymes can become irreversibly inhibited by way of a suicide inactivation by resorcinol [F61][L2747].

It is believed that the Fe3+ of the porphyrin residue of the peroxidase to is oxidised to Fe4+ by hydrogen peroxide with the transfer of an oxygen radical [F61][L2747]. In LPO and TPO, the resulting π-cation radical of the porphyrin can isomerize to a radical cation with the radical in an aromatic side chain of the enzyme [F61][L2747]. The latter radical can bind, in a pH-dependent reaction, covalently and irreversibly to the resorcinol radical formed during regular oxidation of resorcinol and this reduces the activity of the enzyme greatly [F61][L2747]. While the inactivation of the enzyme and the binding of resorcinol to the enzyme may be largely increased by the presence of 0.1 nM iodide, increasing the iodide concentration to 5 mM reduced the resorcinol binding to the enzyme by one quarter but increased the enzyme activity, determined as the rate of iodination of tyrosine, more than proportionally from 6.2% to 44.7% [F61][L2747]. Nevertheless, the role played by iodide ions in the irreversible inactivation of the enzymes is not yet fully elucidated [F61][L2747].

Ultimately, such in vitro and in vivo data propose that the anti-thyroidal activity of resorcinol is caused by inhibition of thyroid peroxidase enzymes, resulting in decreased thyroid hormone production and increased proliferation due to an increase in the secretion of TSH (thyroid stimulating hormone) [F61][L2747]. The iodination process is catalyzed by a haem-containing enzyme, and resorcinol is known to form covalent bonds with haem [F61][L2747].

Despite the legitimacy of this pharmacodynamic profile in resorcinol, the therapeutic uses for which it may be formally indicated for at this time do not actually rely upon any of these mechanisms or dynamics, which are primarily elicited only upon systemic exposure to resorcinol or particularly high overdosage of the agent. This is especially true, considering resorcinol is most commonly available as topical applications to the public.