Abstract
Phototoxicity of fluoroquinolones is connected with oxidative stress induction. Lomefloxacin (8-halogenated derivative) is considered the most phototoxic fluoroquinolone and moxifloxacin (8-methoxy derivative) the least. Melanin pigment may protect cells from oxidative damage. On the other hand, fluoroquinolone–melanin binding may lead to accumulation of drugs and increase their toxicity to skin. The study aimed to examine the antioxidant defense system status in normal melanocytes treated with lomefloxacin and moxifloxacin and exposed to UV-A radiation. The obtained results demonstrated that UV-A radiation enhanced only the lomefloxacin-induced cytotoxic effect in tested cells. It was found that fluoroquinolones alone and with UV-A radiation decreased superoxide dismutase (SOD) activity and SOD1 expression. UV-A radiation enhanced the impact of moxifloxacin on hydrogen peroxide-scavenging enzymes. In turn, lomefloxacin alone increased the activity and the expression of catalase (CAT) and glutathione peroxidase (GPx), whereas UV-A radiation significantly modified the effects of drugs on these enzymes. Taken together, both analyzed fluoroquinolones induced oxidative stress in melanocytes, however, the molecular and biochemical studies indicated the miscellaneous mechanisms for the tested drugs. The variability in phototoxic potential between lomefloxacin and moxifloxacin may result from different effects on the antioxidant enzymes.
Highlights
Adverse cutaneous drug reactions frequently occur in clinical practice
The influence of fluoroquinolones on melanocyte viability was evaluated by the WST-1 test
Lomefloxacin did not affect cell viability in a concentration range from 0.001 mM to 0.01 mM, whereas in concentrations of 0.05 mM, 0.1 mM, 0.5 mM, and 1.0 mM it caused a decrease in cell viability by about 13%, 16%, 33%, and 42%, respectively (Figure 1A)
Summary
Adverse cutaneous drug reactions frequently occur in clinical practice. It has been reported that a lot of widely used drugs cause photosensitivity reactions [2]. A photosensitizer molecule in the singlet excited state reacts directly with cellular macromolecules and organelles, leading to cell damage. A molecule may be in the triplet excited state which is more stable and has a much longer lifetime [5,6]. The phototoxic action of a molecule in the triplet excited state may result from the following events: (i) formation of singlet oxygen through the energy transfer from the excited photosensitizer to molecular oxygen, or (ii) production of reactive oxygen species (ROS) superoxide anion, hydrogen peroxide, or hydroxyl radical through electron or hydrogen transfer [7]
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