Thua-nao, or Thai fermented soybeans, is a traditional Lanna fermented food in Northern Thailand. It is produced by using a specific bacterial species called Bacillus subtilis var. Thua-nao. We investigated the antioxidant activity and cytotoxic effect of isoflavones from Thua-nao. The phenolic compound contents and total flavonoid contents were determined by spectrophotometry. The antioxidant activity was examined using the ABTS, FRAP, and DPPH assays. The isoflavone contents and phenolic compositions were examined by the high-performance liquid chromatography (HPLC) and liquid chromatography-mass spectrometry (LC-MS) techniques. The ability of isoflavones to inhibit human cancer cell growth was assessed by the MTT assay. The total phenolic content, total flavonoid content, and antioxidant activities of the isoflavones were 49.00 ± 0.51 mg GAE/g of dry extract (DE), 10.76 ± 0.82 mg QE/g of DE, 61.03 ± 0.97 µmol Trolox/g of DE, 66.54 ± 3.97 µM FeSO₄/g of DE, and 22.47 ± 1.92% of DPPH inhibition, respectively. Additionally, the isoflavone extracts from Thua-nao had high isoflavone contents and polyphenolic compound compositions, especially daidzein and genistein. The isoflavone demonstrated a weak inhibition of MCF-7 and HEK293 cancer cell growth. It has a high antioxidant component, which is beneficial and can be developed for new therapeutic uses. However, further studies on the benefits of Thua-nao should be performed for realizing better and more effective uses soon.

Iron is essential for numerous biological processes; however, an iron imbalance can contribute to a number of diseases. An excess of iron can accumulate in the body and subsequently induce the production of reactive oxygen species (ROS), leading to oxidative tissue damage and organ dysfunction. The liver, a major iron storage site, is vulnerable to this iron-induced oxidative damage; however, this issue can be overcome by the chelation of excess iron. This study aimed to investigate the effect of 6-gingerol-rich ginger (Zingiber officinale) extract on iron chelation, antioxidation, and hepatoprotective function in protecting against iron-induced oxidative liver cell injury. In experiments, 6-gingerol was confirmed to be a main bioactive component of the ginger extract and possessed free radical scavenging activity, decreasing ABTS^•+ and DPPH^• radical levels, and inhibiting AAPH-induced red blood cell hemolysis. Interestingly, the extract significantly reduced the levels of labile cellular iron (LCI), intracellular ROS, and lipid peroxidation products (TBARS) in iron-loaded human hepatoma (Huh7) cells. In conclusion, this work highlights the iron chelation property of 6-gingerol-rich ginger extract and its antioxidant activity, which could potentially protect the liver from iron-induced oxidative tissue damage.

Background/Objective: Ferroptosis is an iron-dependent form of programmed cell death characterized by lipid peroxidation products (LPOs). A chemotherapeutic drug, 5–fluorouracil (5–FU), can induce epithelial mucositis and favor drug synergism with erastin in ferroptosis. Camellia tea saponin extract (TS) is known to exert antioxidative properties. This study aims to delineate the protective role of TS in mitigating 5–FU-induced ferroptosis and inflammation in human keratinocytes. Methods: HaCaT cells were induced by 5–FU and erastin, treated with different TS doses, and their viability was then determined. Levels of cellular reactive oxygen species (ROS), LPOs, labile iron pool (LIP), glutathione (GSH), glutathione peroxidase 4 (GPX–4) activity, as well as IL–6, IL–1β, and TNF–α levels, and their wound healing properties were assessed. Results: TS per se (at up to 25 µg/mL) was not toxic to HaCaT cells but was unable to restore the viability of 5–FU-induced cells up to the baseline levels. The compound significantly diminished increases in cellular ROS, LPOs, and LIP, while restoring GSH content and GPX–4 activity. Additionally, it suppressed the cytokine production of 5–FU-induced cells in a concentration–dependent manner. Moreover, TS exerted wound-healing effects against skin injuries and 5–FU damage significantly and dose dependently. Conclusions: The insights of this work have identified biochemical mechanisms using tea saponin extract to protect against 5–FU-induced keratinocyte ferroptosis and inflammation. This study highlights the promising adjunctive potential of tea saponin in the mitigation and management of chemotherapy-induced mucositis.

This study aimed to develop perilla fruit oil (PFO)-fortified soybean milk (PFO-SM), identify its sensory acceptability, and evaluate its health outcomes. Our PFO-SM product was pasteurized, analyzed for its nutritional value, and had its acceptability assessed by an experienced and trained descriptive panel (n = 100) based on a relevant set of sensory attributes. A randomized clinical trial was conducted involving healthy subjects who were assigned to consume deionized water (DI), SM, PFO-SM, or black sesame-soybean milk (BS-SM) (n = 48 each, 180 mL/serving) daily for 30 d. Accordingly, health indices and analyzed blood biomarkers were recorded. Consequently, 1% PFO-SM (1.26 mg ALA rich) was generally associated with very high scores for overall acceptance, color, flavor, odor, taste, texture, and sweetness. We observed that PFO-SM lowered levels of serum triglycerides and erythrocyte reactive oxygen species, but increased phagocytosis and serum antioxidant activity (p < 0.05) when compared to SM and BS-SM. These findings indicate that PFO supplementation in soybean milk could enhance radical-scavenging and phagocytotic abilities in the blood of healthy persons. In this regard, it was determined to be more efficient than black sesame supplementation. We are now better positioned to recommend the consumption of PFO-SM drink for the reduction of many chronic diseases. Randomized clinical trial registration (Reference number 41389) by IRSCTN Registry.

A high amount of iron in β-thalassemia patients can lead to oxidative stress and organ dysfunction, especially liver, the main iron accumulated organ. Iron catabolism causes the generation of reactive oxygen species (ROS), triggering liver inflammation, fibrosis, and cirrhosis. Deferiprone-resveratrol hybrid (DFP-RVT) is chemically synthesized by combining deferiprone (DFP) and resveratrol (RVT) which shows an iron-chelating property along with antioxidant activity. This study explored the hepatoprotective effect of DFP-RVT in iron overloaded β-knockout (BKO) thalassemic mice. The results revealed that DFP-RVT treatment improved liver function in iron-overloaded BKO mice by reducing liver enzymes and increasing hepcidin levels compared to iron overload control mice. Both DFP alone and DFP-RVT treatment groups demonstrated iron chelation effects by decreasing liver iron content (LIC), iron profiles, and iron deposition in the liver. Moreover, DFP-RVT powerfully showed antioxidant properties by decreasing liver and plasma thiobarbituric acid reactive substances (TBARs) and increasing reduced glutathione (GSH) and superoxide dismutase (SOD). Interestingly, transforming growth factor β1 (TGFβ1), which can contribute to chronic liver disease through liver injury, inflammation, fibrosis, and cirrhosis, is highly expressed in iron-overloaded mice. However, both DFP and DFP-RVT treatment significantly reduced TGFβ1 levels compared to the iron-overloaded group. Therefore, DFP-RVT could be a potent hepatoprotective compound through the mobilization of iron, reduction of ROS, improvement of liver enzymes, and alleviation of liver damage, potentially relieving liver dysfunction in iron-overloaded BKO mice.

Iron is a crucial trace element and essential for many cellular processes; however, excessive iron accumulation can induce oxidative stress and cell damage. Neurodegenerative disorders, such as Alzheimers disease and Parkinsons disease, have been associated with altered iron homoeostasis causing altered iron distribution and accumulation in brain tissue. This study aims to investigate the protective effect of 1-(N-acetyl-6-aminohexyl)-3-hydroxy-2-methylpyridin-4-one (CM1) in combination with green tea extract (GTE) on iron-induced oxidative stress in neuroblastoma (SH-SY5Y) cells. Cells were cultured in medium with or without ferric chloride loading. Their viability and mitochondrial activity were assessed using MTT and JC-1 staining methods. Levels of the cellular labile iron pool (LIP), reactive oxygen species (ROS), and lipid-peroxidation products were determined using calcein acetoxymethyl ester, 2,7-dichlorohydrofluorescein diacetate, and TBARS-based assays, respectively. The viability of iron-loaded cells was found to be significantly increased after treatment with CM1 (10µM) for 24h. CM1 co-treatment with GTE resulted in a greater protective effect than their monotherapy. Combination of CM1 and GTE also reduced mitochondrial disruption and LIP content and ROS and TBARS production. In conclusion, the combination of CM1 and GTE exhibits protection against iron-induced oxidative stress in neuroblastoma cells.