Antioxidants最新文献

{"title":"Attenuating Effect of a Polyphenol Ellagic Acid on Ovarian Aging by Inhibiting the Ferroptosis Pathway in Low-Yield Laying Chickens.","authors":"Qiongyu Yuan, Xinyu Wang, Yingyu Xiao, Zhaoyu Yang, Xiangyu Cai, Wanyue Gao, Yuling Mi, Caiqiao Zhang","doi":"10.3390/antiox14050614","DOIUrl":"https://doi.org/10.3390/antiox14050614","url":null,"abstract":"<p><p>Aging leads to ovarian degeneration in poultry, reducing egg production and quality. Ellagic acid (EA), a natural plant-derived compound, may help delay ovarian aging, though its precise mechanisms remain unclear. This study investigated the effects of EA on ovarian aging of low-yield laying chickens and explored its underlying mechanism. EA supplementation (100 and 500 mg/kg) significantly increased ovarian weight as well as the number and proportion of small yellow follicles in aging chickens. EA administration elevated serum antioxidant levels and upregulated the expression of glutathione peroxidase 4 (GPX4) expression to reduce oxidative stress. Importantly, EA treatment suppressed the mRNA and protein expression of ferroptosis markers transferrin receptor protein 1 (TFRC) and solute carrier family 7 member 11 (SLC7A11), increased Proliferating Cell Nuclear Antigen (PCNA) expression, and alleviated G1 phase arrest in granulosa cells (GCs), promoting cell proliferation, which improves egg quality and production. Furthermore, in vitro experiments demonstrated that EA treatment decreased reactive oxygen species production, improved mitochondrial function, inhibited ferroptosis, and attenuated GCs aging. In conclusion, this study reveals the critical role of ferroptosis in chicken ovarian aging and suggests that EA may provide a promising approach for delaying ovarian aging and enhancing productivity in low-yield poultry.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-Specific Antioxidant and Anti-Inflammatory Protective Effects of AMPK in Cardiovascular Diseases.","authors":"Lea Strohm, Dominika Mihalikova, Alexander Czarnowski, Zita Schwaibold, Andreas Daiber, Paul Stamm","doi":"10.3390/antiox14050615","DOIUrl":"https://doi.org/10.3390/antiox14050615","url":null,"abstract":"<p><p>Cardiovascular diseases such as coronary heart disease, heart failure, or stroke are the most common cause of death worldwide and are regularly based on risk factors like diabetes mellitus, hypertension, or obesity. At the same time, both diseases and risk factors are significantly influenced by sex hormones. In order to better understand this influence and also specifically improve the therapy of female patients, medical research has recently focused increasingly on gender-specific differences. The goal is to develop personalized, gender-specific therapy concepts for these diseases to further enhance health outcomes. The enzyme adenosine monophosphate-activated protein kinase (AMPK) is a central regulator of energy metabolism, protecting the cardiovascular system from energy depletion, thereby promoting vascular health and preventing cellular damage. AMPK confers cardioprotective effects by preventing endothelial and vascular dysfunction, and by controlling or regulating oxidative stress and inflammatory processes. For AMPK, sex-specific effects were reported, influencing metabolic and cardiovascular responses. Exercise and metabolic stress generally cause higher AMPK activity in males. At the same time, females exhibit protective mechanisms against insulin resistance or oxidative stress, particularly in conditions like obesity. Additionally, males subject to AMPK deficiency seem to experience greater cardiac and mitochondrial dysfunction. In contrast, females show improvement in cardiovascular function after pharmacological AMPK activation. These differences, influenced by hormones, body composition, and gene expression, highlight the potential to develop personalized, sex-specific AMPK-targeted therapeutic strategies for cardiovascular diseases in the future. Here, we discuss the most actual scientific background, focusing on the protective, gender-specific effects of AMPK, and highlight potential clinical applications.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rutaecarpine Protects Human Endothelial Cells from Oxidative-Stress-Induced Apoptosis via TRPV1- and AhR-Mediated Nrf2 Activation.","authors":"Chae Yeon Kim, Gi Ho Lee, Seung Yeon Lee, Anh Thi Ngoc Bui, Hye Gwang Jeong","doi":"10.3390/antiox14050616","DOIUrl":"https://doi.org/10.3390/antiox14050616","url":null,"abstract":"<p><p>Endothelial cells play a crucial role in cardiovascular health by maintaining vascular homeostasis, regulating blood flow and vascular wall permeability, and protecting against external stressors. Oxidative stress, particularly excessive reactive oxygen species (ROS), disrupts cellular homeostasis and contributes to endothelial cell dysfunction. Rutaecarpine (RUT), an indolopyridoquinazolinone alkaloid isolated from <i>Evodia rutaecarpa</i>, has cytoprotective potential. However, the molecular mechanism underlying its cytoprotective activity in endothelial cells remains unclear. In this study, we investigated the protective effects of RUT against H₂O₂-induced apoptosis in human EA.hy926 endothelial cells and explored its underlying mechanism of action. RUT enhanced nuclear factor erythroid 2-related factor 2 (Nrf2) activation by increasing its expression and phosphorylation, resulting in the upregulation of antioxidant enzymes (GCLC, NQO1, and HO-1). RUT increased the level of the anti-apoptotic marker (Bcl-2) while inhibiting apoptotic markers (cleaved caspase-3 and Bax) in H₂O₂-induced apoptotic cells. Mechanistic analysis revealed that RUT activates Nrf2 through two pathways: TRPV1-mediated PKCδ/Akt phosphorylation and aryl hydrocarbon receptor (AhR)-dependent Nrf2 expression. These findings suggest that RUT exerts protective effects against oxidative-stress-induced apoptosis by controlling the Nrf2 signaling pathway in endothelial cells.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155694","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"c-Abl/TFEB Pathway Activation as a Common Pathogenic Mechanism in Lysosomal Storage Diseases: Therapeutic Potential of c-Abl Inhibitors.","authors":"Miguel V Guerra, Juan Castro, Antonio Moreno, Elisa Balboa, Juan J Marugan, Alejandra R Alvarez, Silvana Zanlungo","doi":"10.3390/antiox14050611","DOIUrl":"https://doi.org/10.3390/antiox14050611","url":null,"abstract":"<p><p>Lysosomal storage diseases (LSDs) are characterized by the accumulation of undegraded substrates within lysosomes, often associated with oxidative stress and impaired lysosomal function. In this study, we investigate the role of the c-Abl/TFEB pathway in different LSDs: Gaucher, Niemann-Pick type A (NPA), and Niemann-Pick type C (NPC). Our findings identify c-Abl activation (p-c-Abl) as a common pathogenic mechanism in these disorders. We demonstrate that c-Abl phosphorylates TFEB at Tyr173, leading to its cytoplasmic retention. Using pharmacological models of Gaucher, NPA and NPC in SH-SY5Y neuronal cells and HeLa cells, we assess the effects of the c-Abl inhibitors Imatinib and Neurotinib, as well as the antioxidant α-Tocopherol (α-TOH), on TFEB nuclear translocation and p-c-Abl protein levels. Additionally, we explore the effects of c-Abl inhibitors in cholesterol accumulation in LSDs neuronal models. Our results show that treatment with c-Abl inhibitors or α-TOH promotes TFEB nuclear translocation, enhances lysosomal clearance, and reduces cholesterol accumulation in all three LSD models. These findings highlight the c-Abl/TFEB pathway as a potential therapeutic target for LSDs and potentially other neurodegenerative disorders associated with lysosomal dysfunction.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Ferroptosis-Mitochondrial Axis in Depression: Unraveling the Feedforward Loop of Oxidative Stress, Metabolic Homeostasis Dysregulation, and Neuroinflammation.","authors":"Xu Liu, Qiang Luo, Yulong Zhao, Peng Ren, Yu Jin, Junjie Zhou","doi":"10.3390/antiox14050613","DOIUrl":"https://doi.org/10.3390/antiox14050613","url":null,"abstract":"<p><p>Emerging evidence links ferroptosis-mitochondrial dysregulation to depression pathogenesis through an oxidative stress-energy deficit-neuroinflammation cycle driven by iron overload. This study demonstrates that iron accumulation initiates ferroptosis via Fenton reaction-mediated lipid peroxidation, compromising neuronal membrane integrity and disabling the GPx4 antioxidant system. Concurrent mitochondrial complex I/IV dysfunction impairs ATP synthesis, creating an AMPK/mTOR signaling imbalance and calcium dyshomeostasis that synergistically impair synaptic plasticity. Bidirectional crosstalk emerges: lipid peroxidation derivatives oxidize mitochondrial cardiolipin, while mitochondrial ROS overproduction activates ACSL4 to amplify ferroptotic susceptibility, forming a self-reinforcing neurodegenerative loop. Prefrontal-hippocampal metabolomics reveal paradoxical metabolic reprogramming with glycolytic compensation suppressing mitochondrial biogenesis (via PGC-1α/TFAM downregulation), trapping neurons in bioenergetic crisis. Clinical data further show that microglial M1 polarization through cGAS-STING activation sustains neuroinflammation via IL-6/TNF-α release. We propose a \"ferroptosis-mitochondrial fragmentation-metabolic maladaptation\" triad as mechanistic subtyping criteria for depression. Preclinical validation shows that combinatorial therapy (iron chelators + SIRT3 agonists) rescues neuronal viability by restoring mitochondrial integrity and energy flux. This work shifts therapeutic paradigms from monoaminergic targets toward multimodal strategies addressing iron homeostasis, organelle dynamics, and metabolic vulnerability-a framework with significant implications for developing neuroprotective antidepressants.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155875","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardio-Renal and Systemic Effects of SGLT2i Dapagliflozin on Short-Term Anthracycline and HER-2-Blocking Agent Therapy-Induced Cardiotoxicity.","authors":"Vincenzo Quagliariello, Annabella Di Mauro, Gerardo Ferrara, Francesca Bruzzese, Giuseppe Palma, Antonio Luciano, Maria Laura Canale, Irma Bisceglia, Martina Iovine, Christian Cadeddu Dessalvi, Carlo Maurea, Matteo Barbato, Alessandro Inno, Massimiliano Berretta, Andrea Paccone, Alfredo Mauriello, Celeste Fonderico, Anna Chiara Maratea, Nicola Maurea","doi":"10.3390/antiox14050612","DOIUrl":"https://doi.org/10.3390/antiox14050612","url":null,"abstract":"<p><p>Anthracyclines and human epidermal growth factor receptor 2 (HER-2) inhibitors are cornerstone therapies for breast cancer but are associated with significant cardiotoxicity. While sodium-glucose cotransporter 2 (SGLT2) inhibitors such as dapagliflozin have demonstrated cardio-renal protective effects during anthracycline treatment, their efficacy in preventing cardiotoxicity from sequential anthracycline and HER-2 blockade remains poorly understood. This study investigates the cardioprotective role of dapagliflozin in a preclinical model of chemotherapy-induced cardiotoxicity. Female C57Bl/6 mice were divided into four groups and treated for 10 days as follows: (1) a normal control group receiving saline (sham); (2) a model control group receiving doxorubicin (2.17 mg/kg/day for 5 days) followed by HER-2-blocking monoclonal antibody (2.25 mg/kg/day for 5 days); (3) a dapagliflozin-only group (10 mg/kg/day via oral gavage); and (4) a treatment group receiving the combination of doxorubicin, HER-2 inhibitor, and dapagliflozin. Cardiac function was assessed using echocardiography (VEVO 2100). Biomarkers of myocardial injury and inflammation (NLRP3, MyD88, CXCR4, H-FABP, troponin-T, and cytokines) were quantified via ELISA and immunohistochemistry. Circulating markers such as mitofusin-2, cardiac myosin light chain, malondialdehyde (MDA), and 4-hydroxy-2-nonenal (4-HNE) were also measured. Dapagliflozin significantly preserved the ejection fraction and reduced both radial and longitudinal strain impairment in mice treated with the doxorubicin-HER-2 inhibitor combination (<i>p</i> < 0.001). Levels of myocardial NLRP3, MyD88, CXCR4, H-FABP, interleukin-1β, and troponin-T were significantly lower in the dapagliflozin-treated group compared to the chemotherapy-only group. Serum markers of oxidative stress and cardiac injury, including mitofusin-2, MDA, 4-HNE, BNP, and high-sensitivity C-reactive protein (hs-CRP), were also reduced by dapagliflozin treatment. Our findings demonstrate that dapagliflozin effectively mitigates early cardiac dysfunction and injury in a preclinical model of sequential doxorubicin and HER-2 inhibitor therapy.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155789","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-Inflammasome Effect of Impressic Acid on Diesel Exhaust Particulate Matter-Induced NLRP1 Inflammasome via the Keap1/p62/Nrf2-Signaling Pathway in Keratinocytes.","authors":"Seung Yeon Lee, Gi Ho Lee, Jeonghwan Maeng, Su Yeon Kim, Hwi-Yeol Yun, Gil-Saeng Jeong, Hye Gwang Jeong","doi":"10.3390/antiox14050610","DOIUrl":"https://doi.org/10.3390/antiox14050610","url":null,"abstract":"<p><p>Diesel exhaust particulate (DEP) is widely recognized to weaken lung function and skin diseases. When the skin, which defends against external factors, is exposed to PM2.5, various chronic inflammatory diseases occur. When keratinocytes recognize harmful signals, they synthesize the NOD-like receptor protein 1 (NLRP1) inflammasome. DEP enhances NF-κB signaling and NLRP1 inflammasome expression through the interaction of TXNIP with NLRP1 in keratinocytes. Although many studies have reported the anti-inflammatory and antioxidant characteristics of Impressic acid (IPA), the umbrella consequences of IPA for PM2.5-influenced inflammasomes and the associated mechanisms remain unknown. Therefore, this study aimed to examine the protective function of IPA against inflammation in human keratinocytes. IPA attenuated the NLRP1 expression, caspase-1, IL-1β actuation, and NF-κB and IκB phosphorylation induction by DEP. IPA upregulated the Nrf2, HO-1, and NQO1 expression through CaMKKβ, AMPK, and GSK3β phosphorylation. Also, IPA led to the elevation of p62 and the degradation of the Keap1 protein. ML385 reversed the suppressive effect of IPA on the NLRP1 inflammasome, which was enhanced by DEP, and NAC counteracted the effect of ML385. These findings indicate that IPA can suppress inflammation induced by PM2.5 by expressing antioxidant enzymes through the Keap1/p62/Nrf2-signaling pathway in human keratinocytes.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alleviating the Effect of Branched-Chain Fatty Acids on the Lipopolysaccharide-Induced Inflammatory Response in Calf Small Intestinal Epithelial Cells.","authors":"Siqi Zhang, Qingyuan Yu, Yukun Sun, Guangning Zhang, Yonggen Zhang, Hangshu Xin","doi":"10.3390/antiox14050608","DOIUrl":"https://doi.org/10.3390/antiox14050608","url":null,"abstract":"<p><p>This study examined branched-chain fatty acids (BCFAs)' effects on oxidative stress, energy metabolism, inflammation, tight junction disruption, apoptosis, and Toll-like receptor 4/nuclear factor kappa-B (<i>TLR4/NF-κB</i>) signaling in lipopolysaccharide (LPS)-induced calf small intestinal epithelial cells (CSIECs). Eight groups were used: a control group, an LPS-induced group, and six BCFA treatment groups (12-methyltridecanoic acid (iso-C14:0), 13-methyltetradecanoic acid (iso-C15:0), 14-methylpentadecanoic acid (iso-C16:0), 15-methylhexadecanoic acid (iso-C17:0), 12-methyltetradecanoic acid (anteiso-C15:0), and 14-methylhexadecanoic acid (anteiso-C17:0)) with LPS. The BCFA pretreatments significantly increased CSIEC activity compared to the LPS-induced group, with iso-C14:0 showing the highest activity (89.73%). BCFA reduced Reactive Oxygen Species (ROS) generation and malondialdehyde (MDA) levels and improved the superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities and glutathione (GSH) levels. Iso-C16:0 optimized total antioxidant capacity (T-AOC). BCFA enhanced the mitochondrial membrane potential, Adenosine Triphosphate (ATP) enzyme activity, and ATP content, with iso-C14:0 increasing ATP by 27.01%. BCFA downregulated interleukin (<i>IL</i>)<i>-1β</i>, <i>IL-8</i>, tumor necrosis factor (<i>TNF</i>)-<i>α</i>, and interferon (<i>INF</i>)-<i>γ</i> gene expression, reduced IL-6 levels, and increased <i>IL-10</i> expression. Myeloid differentiation factor 88 (<i>MyD88</i>) mRNA levels were reduced. BCFA alleviated Zonula Occludin (<i>ZO-1</i>), <i>Claudin-1</i>, and <i>Claudin-4</i> decrease and increased Occludin levels. BCFA mitigated LPS-induced increases in <i>Caspase-3</i> and BCL2-Associated X (<i>BAX</i>) mRNA levels, reduced <i>Caspase-8</i> and <i>Caspase-9</i> expression, and increased B-Cell Lymphoma-2 (<i>BCL-2</i>) mRNA levels. The Entropy Weight-TOPSIS method was adopted, and it was discovered that iso-C15:0 has the best effect. In summary, BCFA supplementation mitigated oxidative stress and enhanced mitochondrial function. BCFA inhibited <i>TLR4/NF-κB</i> signaling pathway overactivation, regulated inflammatory cytokine gene expression, reduced cellular apoptosis, preserved tight junction integrity, and supported barrier function.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effectiveness of Astaxanthin as a Feed Supplement to Improve Growth Performance and Feed Utilization in Aquaculture Animals: A Meta-Analysis.","authors":"Bowen Li, Chunxiu Chen, Xiaoqing Zhou, Huiru Liu, Zhixiong Zhou, Xiaoyu Wang, Jian Liang, Yongjun Guo, Shuang Liang","doi":"10.3390/antiox14050609","DOIUrl":"https://doi.org/10.3390/antiox14050609","url":null,"abstract":"<p><p>Aquaculture, a vital component of global food supply, faces challenges from environmental stressors that compromise aquatic animal health and productivity. Astaxanthin, a potent carotenoid antioxidant, has shown promise in enhancing growth and stress resilience in aquaculture species, yet its effects remain inconsistent across studies. This meta-analysis systematically evaluates the efficacy of dietary astaxanthin supplementation on growth, feed utilization, antioxidant capacity, and immune function in aquaculture animals. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, 64 studies (33 species, 964 comparisons) published prior to 2025 were analyzed using a random-effects model. Results demonstrated that astaxanthin significantly improved final body weight, weight gain rate, specific growth rate, survival rate, and protein efficiency ratio, while reducing feed conversion ratio. Additionally, it enhanced digestive enzyme activities, hepatopancreas antioxidant biomarkers, and immune parameters. The subgroup analysis revealed differences related to species, trophic level, and habitat, and estimated the optimal dose for key indicators. Despite heterogeneity and publication bias, adjusted effect sizes remained significant for most outcomes. These findings underscore astaxanthin's potential as a multifunctional feed additive to promote sustainable aquaculture, though its efficacy depends on species, dosage, and environmental context, warranting further mechanistic and optimization studies.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155799","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Geochemical Speciation, Uptake, and Transportation Mechanisms of Arsenic, Cadmium, and Lead in Soil-Rice Systems: Additional Aspects and Challenges.","authors":"Chaw Su Lwin, Ha-Il Jung, Myung-Sook Kim, Eun-Jin Lee, Tae-Gu Lee","doi":"10.3390/antiox14050607","DOIUrl":"https://doi.org/10.3390/antiox14050607","url":null,"abstract":"<p><p>Potentially toxic elements (PTE), such as cadmium (Cd), lead (Pb), and arsenic (As), threaten rice (<i>Oryza sativa</i> L.) crop productivity and pose significant risks to human health when they are present in soil. This review summarizes the current understanding of soil and rice contamination with As, Cd, and Pb to provide an in-depth understanding of the dynamics of these contaminants and the mechanisms regulating their flow from soil to plants. It focuses on the following aspects: (1) these metals' geochemical distribution and speciation in soil-rice systems; (2) factors influencing the transformation, bioavailability, and uptake of these metals in paddy soils; (3) metal uptake, transport, translocation, and accumulation mechanisms in rice grains; and (4) the roles of transporters involved in metal uptake, transport, and accumulation in rice plants. Moreover, this review contributes to a clearer understanding of the environmental risks associated with these toxic metals in soil-rice ecosystems. Furthermore, it highlights the challenges in simultaneously managing the risks of As, Cd, and Pb contamination in rice. The study findings may help inspire innovative methods, biotechnological applications, and sustainable management strategies to mitigate the accumulation of As, Cd, and Pb in rice grains while effectively addressing multi-metal contamination in paddy soils.</p>","PeriodicalId":7984,"journal":{"name":"Antioxidants","volume":"14 5","pages":""},"PeriodicalIF":6.0,"publicationDate":"2025-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144155707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}