Key result
Nine respiratory drugs potently inhibited human serum paraoxonase-1 at the micromolar level, with IC50 values ranging from 0.219 μM (salbutamol sulfate) to 67.205 μM (montelukast sodium).
Effect estimate: IC50 0.219 to 67.205 μM
Several commonly used respiratory drugs are potent inhibitors of human serum paraoxonase-1 in vitro.
Respiratory drugs may alter hPON1 activity; leaves open any clinical relevance to drug safety or outcomes.
In this study, we investigated the effects of certain respiratory drugs, which are mainly used on human serum paraoxonase‐1 (hPON1; EC 3.1.8.1). hPON1 was purified from human serum, with 354.91 fold and 45% yield by using two simple step procedures including, first, ammonium sulfate precipitation, then, Sepharose‐4B‐l‐tyrosine‐1‐naphthylamine hydrophobic interaction chromatography. SDS‐polyacrylamide gel electrophoresis showed a single protein band belonging to hPON1 with 43 kDa. All the pharmaceutical compounds inhibited the PON1 enzyme highly at the micromolar level. The obtained IC50 values for nine different pharmaceutics ranged from 0.219 μM (salbutamol sulfate) to 67.205 μM (montelukast sodium). So, all drugs could be considered as potent hPON1 inhibitors. Ki values and inhibition types were determined by Lineweaver‐Burk graphs. While varenicline tartrate and moxifloxacin hydrochloride inhibited the enzyme in a noncompetitive manner, others inhibited it in a mixed manner.
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Gökçe et al. (2019) studied this question. Respiratory drugs (including salbutamol sulfate, montelukast sodium, varenicline tartrate, moxifloxacin hydrochloride) was evaluated on Inhibition of hPON1 enzyme (IC50 and Ki values) (IC50 0.219 to 67.205 μM). Nine respiratory drugs potently inhibited human serum paraoxonase-1 at the micromolar level, with IC50 values ranging from 0.219 μM (salbutamol sulfate) to 67.205 μM (montelukast sodium).
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