{"i":"Ferritinophagy","sup":["+","tf"],"#text":"Melatonin Attenuates/Ferroptosis by Acting on Autophagy in the Liver of an Autistic Mouse Model BTBR TItpr3/J."}

Scientists studied how melatonin affects liver health in mice that model autism-like behaviors. These mice had liver problems including abnormal protein clumps and damaged cell cleanup systems. When given melatonin, the mice showed healthier liver tissue and better cellular function. This suggests melatonin might help protect liver health, though more research is needed to understand if this applies to autistic people.

This preclinical study investigated melatonin's effects on liver function in BTBR mice, an established autism animal model. Researchers examined liver tissue architecture and measured markers of autophagy (cellular cleanup processes) and ferroptosis (iron-dependent cell death). BTBR mice showed liver abnormalities including cytoplasmic inclusions called Mallory-Denk bodies, impaired autophagy, and increased ferroptosis compared to controls. Melatonin treatment improved liver morphology, enhanced autophagy function, and reduced ferroptosis.

The study suggests melatonin may protect liver function by promoting cellular cleanup mechanisms and preventing iron-mediated cell damage in this autism mouse model.

While preliminary, this research suggests melatonin may have broader protective effects beyond sleep in autism. However, these liver findings in mice require human studies before clinical application. Current melatonin use for sleep issues in autism appears supported separately.

Animal model findings may not translate to humans. Sample size not reported. Single study requiring replication. Liver findings may not reflect brain pathology. Mechanisms unclear regarding relevance to core autism symptoms.

Autism spectrum disorders (ASDs) are a pool of neurodevelopment disorders in which social impairment is the main symptom. Presently, there are no definitive medications to cure the symptoms but the therapeutic strategies that are taken ameliorate them. The purpose of this study was to investigate the effects of melatonin (MLT) in treating ASDs using an autistic mouse model BTBR TItpr3/J (BTBR). We evaluated the hepatic cytoarchitecture and some markers of autophagy,/ferroptosis, in BTBR mice treated and not-treated with MLT.

The hepatic morphology and the autophagy and/ferroptosis pathways were analyzed by histological, immunohistochemical, and Western blotting techniques. We studied p62 and microtubule-associated protein 1 light chain 3 B (LC3B) for evaluating the autophagy; nuclear receptor co-activator 4 (NCOA4) and long-chain-coenzyme synthase (ACSL4) for monitoring/ferroptosis. The liver of BTBR mice revealed that the hepatocytes showed many cytoplasmic inclusions recognized as Mallory-Denk bodies (MDBs); the expression and levels of p62 and LC3B were downregulated, whereas ACSL4 and NCOA4 were upregulated, as compared to control animals. MLT administration to BTBR mice ameliorated liver damage and reduced the impairment of autophagy and/ferroptosis.

In conclusion, we observed that MLT alleviates liver damage in BTBR mice by improving the degradation of intracellular MDBs, promoting autophagy, and suppressing/ferroptosis.