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This Review reconciles the biochemical foundation of ferroptosis, the evidence supporting its role in cancer biology and the potential strategies for rationalizing targeted therapies to induce ferroptosis-prone states in malignancies

Scaglia F, Sutton VR, Bodamer OA, Vogel H, Shapira SK, Naviaux RK, Vladutiu GD

Since the raison detre for a micronutrient prescription is to boost the supply of CH 3 and SH moieties (Section 3), the inefficacy of the micronutrient curcumin (despite curbing lipid peroxidaton and being a potent inhibitor of mast cells) and allopurinol (inhibitor of xanthine oxidase) in clinical trials indicates that these substances do not achieve the goal: of note, curcumin did not increase GSH in erythrocytes

doi: 10.1111/cts.12694 58 HornungNStengaard-PedersenKEhrnroothEEllingsenTPoulsenJH

There is a separate type of steatosis by which phospholipid accumulation leads to a pattern similar to the diseases with inherited phospholipid metabolism defects (e.g., TaySachs disease) Causes: (a) Microvesicular: Aspirin (Reye's syndrome), ketoprofen, tetracycline (especially if expired) (b) Macrovesicular: Acetaminophen, methotrexate (c) Phospholipidosis: Amiodarone, total parenteral nutrition (d) Antiviral: nucleoside analogues (e) Corticosteroid (f) Hormonal: Tamoxifen Granuloma [edit] Drug-induced hepatic granulomas are usually associated with granulomas in other tissues and patients typically have features of systemic vasculitis and hypersensitivity

The dual pathway synergy drives superior weight loss versus pure GLP-1 agonists