The toxicity effect of silver nanoparticles (AgNPs) on growth and cellular viability was investigated on the aquatic plant Lemna gibba exposed over 7 d to 0, 0.01, 0.1, 1, and 10 mg/L of AgNPs. Growth inhibition was demonstrated by a significant decrease of frond numbers dependent on AgNP concentration. Under these conditions, reduction in plant cellular viability was detected for 0.1, 1, and 10 mg/L of AgNPs within 7 d of AgNPs treatment. This effect was highly correlated with the production of intracellular reactive oxygen species (ROS). A significant increase of intracellular ROS formation was triggered by 1 and 10 mg/L of AgNP exposure. The induced oxidative stress was related to Ag accumulation within L. gibba plant cells and with the increasing concentration of AgNP exposure in the medium. The authors' results clearly suggested that AgNP suspension represented a potential source of toxicity for L. gibba plant cells. Due to the low release capacity of free soluble Ag from AgNP dissolution in the medium, it is most likely that the intracellular uptake of Ag was directly from AgNPs, triggering cellular oxidative stress that may be due to the release of free Ag inside plant cells. Therefore, the present study demonstrated that AgNP accumulation in an aquatic environment may represent a potential source of toxicity and a risk for the viability of duckweeds.
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http://dx.doi.org/10.1002/etc.2131 | DOI Listing |
Sci Adv
January 2025
Department of Biochemistry and Molecular Biology, McGovern Medical School, The University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Current dogma assumes that lipid asymmetry in biological membranes is actively maintained and dispensable for cell viability. The inner (cytoplasmic) membrane (IM) of is asymmetric. However, the molecular mechanism that maintains this uneven distribution is unknown.
View Article and Find Full Text PDFJ Nat Med
January 2025
Department of Endocrinology, Cangzhou Central Hospital, No. 16 West Xinhua Road, Cangzhou, 061000, Hebei, China.
Thioredoxin-interacting protein (TXNIP), as a pivotal protein in the cellular stress response, plays a significant role in the progression of diabetic nephropathy (DN). Consequently, therapeutic strategies aimed at targeting TXNIP may offer novel interventions for patients with DN. Our study is to explore the therapeutic potential of targeting TXNIP in mitigating renal tubular injury induced by hyperglycemia.
View Article and Find Full Text PDFNeurochem Res
January 2025
College of Pharmacy, Guangxi Medical University, Guangxi Zhuang Autonomous Region, Nanning, 530021, China.
To study the neuronal protective effect and its potential mechanism of C16 against gp120-induced cognitive impairment in vitro and in vivo. The NORT method was used to evaluate the short-term memory abilities of rats, the morphological changes in hippocampus were observed by Nissl staining. Cell viability and damage degree were detected by MTT and LDH.
View Article and Find Full Text PDFHum Cell
January 2025
Infectious Disease Laboratory, Chengdu Public Health Clinical Center, Chengdu, 610061, People's Republic of China.
Hepatocellular carcinoma (HCC) is a primary malignant neoplasm exhibiting a high mortality rate. Taxifolin is a naturally occurring flavonoid compound that exhibits a range of pharmacological properties. The effects of taxifolin on HCC remain largely unexplored.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
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