Manganese (Mn) toxicity limits plant growth in acid soils. Although Mn toxicity induces oxidative stress, the role of superoxide dismutase (SOD, EC.1.15.1.1) isoforms in conferring Mn tolerance remains unclear. Seedlings of ryegrass cultivars Nui (Mn-sensitive) and Kingston (Mn-tolerant) were hydroponically grown at 2.4 (optimal) or 750 μM Mn (toxic) concentration, and harvested from 2 to 48 h. Kingston showed higher shoot Mn than Nui at 2.4 μM Mn. At toxic supply, shoot Mn concentration steadily increased in both cultivars, with Kingston having the highest accumulation at 48 h. An early (2 h) increase in lipid peroxidation under Mn excess occurred, but it returned (after 6 h) to the basal level in Kingston only. Kingston exhibited higher SOD activity than Nui, and that difference increased due to toxic Mn. In general, Mn-induced gene expression of Mn- and Cu/Zn-SOD isoforms was higher in Nui than Kingston. Nevertheless, under Mn excess, we found a greater Fe-SOD up-regulation (up to 5-fold) in Kingston compared to Nui. Thus, Fe-SOD induction in Kingston might explain, at least partly, its high tolerance to Mn toxicity. This is the first evidence that Mn toxicity causes differential gene expression of SOD isoforms in ryegrass cultivars in the short-term.
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http://dx.doi.org/10.1016/j.plaphy.2013.08.012 | DOI Listing |
Front Biosci (Landmark Ed)
January 2025
Department of Otolaryngology, Head and Neck Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, 330006 Nanchang, Jiangxi, China.
Background: It has been reported the therapeutic effects of mesenchymal stem cells (MSCs) on hearing loss. This study explored the therapeutic effects of growth differentiation factor 6 (GDF6) overexpression-induced MSCs (MSCs-GDF6) on age-related hearing loss (ARHL) and its underlying mechanisms.
Methods: Reverse transcription-quantitative PCR and western blotting were used to evaluate gene expression.
Front Biosci (Landmark Ed)
January 2025
Department of Cardiothoracic Surgery, The Affiliated Jiangyin Hospital of Nantong University, 214400 Jiangyin, Jiangsu, China.
Background: This study investigates the role of small ubiquitin-like modifier (SUMO)-specific peptidase 5 (SENP5), a key regulator of SUMOylation, in esophageal squamous cell carcinoma (ESCC), a lethal disease, and its underlying molecular mechanisms.
Methods: Differentially expressed genes between ESCC mouse oesophageal cancer tissues and normal tissues were analysed via RNA-seq; among them, SENP5 expression was upregulated, and this gene was selected for further analysis. Immunohistochemistry and western blotting were then used to validate the increased protein level of SENP5 in both mouse and human ESCC samples.
Front Biosci (Landmark Ed)
January 2025
Division of Molecular Psychiatry, Center of Mental Health, University of Hospital Würzburg, 97080 Würzburg, Germany.
Background: The inheritance of the short allele, encoding the serotonin transporter (SERT) in humans, increases susceptibility to neuropsychiatric and metabolic disorders, with aging and female sex further exacerbating these conditions. Both central and peripheral mechanisms of the compromised serotonin (5-HT) system play crucial roles in this context. Previous studies on SERT-deficient (Sert) mice, which model human SERT deficiency, have demonstrated emotional and metabolic disturbances, exacerbated by exposure to a high-fat Western diet (WD).
View Article and Find Full Text PDFFront Biosci (Landmark Ed)
January 2025
Department of Chemoradiotherapy, Ningbo No 2 Hospital, 315000 Ningbo, Zhejiang, China.
Background: Breast cancer stem cells (BCSCs) are instrumental in treatment resistance, recurrence, and metastasis. The development of breast cancer and radiation sensitivity is intimately pertinent to long non-coding RNA (lncRNA). This work is formulated to investigate how the lncRNA affects the stemness and radioresistance of BCSCs.
View Article and Find Full Text PDFPharm Biol
December 2025
The Affiliated Hospital, Changchun University of Chinese Medicine, Changchun, China.
Context: The decline in ovarian reserve is a major concern in female reproductive health, often associated with oxidative stress and mitochondrial dysfunction. Although ginsenoside Rg1 is known to modulate mitophagy, its effectiveness in mitigating ovarian reserve decline remains unclear.
Objective: To investigate the role of ginsenoside Rg1 in promoting mitophagy to preserve ovarian reserve.
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