Apomorphine is a potent inhibitor of ferroptosis independent of dopaminergic receptors.

Originally, apomorphine was a broad-spectrum dopamine agonist with an affinity for all subtypes of the Dopamine D1 receptor to the D5 receptor. We previously identified apomorphine as a potential therapeutic agent for mitochondrial diseases by screening a chemical library of fibroblasts from patients with mitochondrial diseases. In this study, we showed that apomorphine prevented ferroptosis in fibroblasts from various types of mitochondrial diseases as well as in normal controls. Well-known biomarkers of ferroptosis include protein markers such as prostaglandin endoperoxide synthase 2 (PTGS2), a key gene for ferroptosis-related inflammation PTGS2, lipid peroxidation, and reactive oxygen species. Our findings that apomorphine induced significant downregulation of PTSG2 and suppressed lipid peroxide to the same extent as other inhibitors of ferroptosis also indicate that apomorphine suppresses ferroptosis. To our knowledge, this is the first study to report that the anti-ferroptosis effect of apomorphine is not related to dopamine receptor agonist action and that apomorphine is a potent inhibitor of ferroptotic cell death independent of dopaminergic receptors.

Field survey of ryanodine receptor mutations (G4946E and I4790K) and their effects on biotic performance in the diamondback moth.

This study examined changes in the proportions of ryanodine receptor mutations (G4946E and I4790K) for Plutella xylostella populations in the field. Results show that the proportion of G4946E decreased during the survey years without diamide application and that insects with I4790K were observed less frequently during the survey period. This study also examined the biotic performances of diamide-resistant P. xylostella strains. The results show that the diamide-resistant strains exhibited hatchability, larval development, and fecundity equivalent to those of diamide-susceptible strains.