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The possible mechanisms of arsenic-induced cardiotoxicity mainly include oxidative stress, DNA fragmentation, changes in cardiac ion channels (Figure 2, the possible arsenic exposure routes and mechanism of natural products against cadmium-induced cardiotoxicity have been summarized

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Whether oral use is appropriate depends on the patients symptoms, product quality, treatment goal, and provider recommendation

By assessing genetic factors related to oxidative stress, DNA damage, lipid metabolism, microbiome health, and methylation, this report provides healthcare practitioners with valuable insights to develop personalized health plans and interventions

Supplementary material The Supplementary Material for this article can be found online at: Abbreviations AQ amodiaquine AQ-SG 5-glutathion- S -yl-amodiaquine AQ-QI amodiaquine-quinoneimine BSO L -buthionine-sulfoximine CDNB 1-chloro-2, 4-dinitrobenzene CYP cytochromes P450 DEAQ N -desethylamodiaquine DEAQ-SG 5-glutathion- S -yl- N -desethylamodiaquine DEAQ-QI N -desethylamodiaquine-quinoneimine DMEM Dulbeccos modified Eagle medium DMF N,N -dimethylformamide ER endoplasmic reticulum FBS fetal bovine serum GSH glutathione GSSG glutathione disulfide GST glutathione S -transferase H 2 O 2 hydrogen peroxide HClO 4 perchloric acid HRP horseradish peroxidase NQO1 NAD(P)H:quinone oxidoreductase 1 NAPQI N -acetyl- p -benzoquinonimine PBS phosphate-buffered saline QI quinoneimine

[1] Patients with diabetes and pre-existing retinopathy should be monitored for worsening retinopathy during rapid improvement in glycemic control