Metallothionein (MT)

• CAS: 9038-94-2
• Catalog Number: ALC-FP-9038942
• Category: Featured Products
• Appearance: Off-white powder
• Drying Loss: ≤ 5.0%
• Mesh Size: 100% pass 80 mesh
• Microbiological Test: Total Plate Count ≤ 1000cfu/g, Conforms; Yeast Mold ≤ 100cfu/g, Conforms; Coliforms ≤ 0.92MPN/g, Negative; E.coil Absent/10g, Negative; Salmonella Absent/25g, Negative; Staphylococcus Absent/10g, Negative
• Residue Analysis: Pb ≤ 3ppm,Conforms; As ≤ 1ppm, Conforms; Hg ≤ 0.1ppm, Conforms; Cd ≤ 1ppm, Conforms
• Sample Lot No.: A24X04191
• Source: Rabbit liver

Case Study

Metallothionein for the Prevention of Air Pollutant-Induced Acute Lung Injury

Tanaka K-I, et al. Biomedicine & Pharmacotherapy, 2025, 185, 117965.

In this study, metallothionein (MT) was evaluated for its protective effect against urban aerosol-induced acute lung injury using metallothionein knockout (MT-KO) and wild-type (WT) mice. Acute lung injury was induced via intratracheal administration of urban aerosols. Bronchoalveolar lavage fluid (BALF) analysis revealed that MT-KO mice exhibited significantly higher inflammatory cell infiltration, total protein, and dsDNA levels compared to WT controls. Lung tissue analyses showed elevated mRNA expression of proinflammatory cytokines (Tnf-α, Il-1β, Il-6) and chemokines (Kc, Mip2) in MT-KO mice following aerosol exposure. Reactive oxygen species (ROS) production, assessed via in vivo chemiluminescence imaging, was 3.1-fold higher in MT-KO lungs relative to WT lungs. Notably, intraperitoneal administration of zinc acetate induced MT expression, reducing inflammatory responses and ROS generation. These findings demonstrate the experimental application of metallothionein as an antioxidant agent mitigating air pollutant-induced pulmonary injury.

Metallothionein for Enhancing Antitumor Evaluation of Isoconazole Nitrate in Hepatocellular Carcinoma

Mo C-F, et al. Chemico-Biological Interactions, 2025, 418, 111614.

This study investigated the role of metallothioneins (MTs) in modulating the antitumor activity of isoconazole nitrate (ISN) in hepatocellular carcinoma (HCC). In vitro, HCC cells were treated with ISN, with or without MT knockdown, and analyzed for proliferation, motility, and ROS generation. Transcriptome sequencing coupled with Gene Ontology enrichment revealed MT family genes as key detoxification responders. NRF2 nuclear translocation and binding to antioxidant response elements were confirmed, linking MT transcription to redox homeostasis. In vivo, HepG2 xenografts in nude mice received intraperitoneal injections of ISN (20 mg/kg) and/or the MT inhibitor PPG (40 mg/kg) every other day. Tumor growth, volume, and proliferation markers (Ki67, cleaved PARP) were measured, alongside lipid peroxidation (MDA). Combined ISN and MT inhibition significantly suppressed tumor progression, demonstrating MTs' protective role and providing a robust experimental framework for enhancing ISN efficacy.