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Some neonicotinoids have been restricted in outdoor environments due to their risks to pollinating insects, yet their safety for non-target organisms in greenhouses is still unknown. This study investigates the deposition, degradation, and metabolic dynamics of thiacloprid on greenhouse-grown tomato and assesses its toxicity risk to pollinating bumblebees from spatial and temporal perspectives. Spatially, thiacloprid initially concentrated in leaves (71 %) and flowers (23 %), with deposition in the upper plant being 1.5 times that of the lower sections. The compound's half-life varied by plant tissue: flowers (3.28 days), fruits (4.04 days), stems (4.13 days), and leaves (10.37 days), with the upper sections 1.05-1.75 times higher than in the lower sections of the same organ. Five primary metabolites were identified in tomato tissues, peaking in leaves and flowers 5-7 days. Additionally, greenhouse thiacloprid exposure affected bumblebee body weight, mortality, and pollinated fruit weight. The risk quotient index further proves that thiacloprid residues in leaves and flowers posed an exposure risk to bumblebees, with risk levels subsiding below threshold values after 5 days in flowers and 21 days in leaves. The findings provide an important reference for the exposure risk and safe use supervision of neonicotinoid insecticides to pollinating insects in greenhouse scenarios.
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http://dx.doi.org/10.1016/j.jhazmat.2025.137897 | DOI Listing |
JCI Insight
September 2025
Diabetes & Metabolism Research Center, University of Utah, Salt Lake City, United States of America.
Impaired muscle regrowth in aging is underpinned by reduced pro-inflammatory macrophage function and subsequently impaired muscle cellular remodeling. Macrophage phenotype is metabolically controlled through TCA intermediate accumulation and activation of HIF1A. We hypothesized that transient hypoxia following disuse in old mice would enhance macrophage metabolic inflammatory function thereby improving muscle cellular remodeling and recovery.
View Article and Find Full Text PDFEur Arch Paediatr Dent
September 2025
Araçatuba School of Dentistry, São Paulo State University - UNESP, Araçatuba, Brazil.
Purpose: This systematic review provides a critical evaluation, synthesis of the existing literature on isotretinoin's effects on craniomaxillofacial bone.
Methods: Following the PRISMA guidelines and registered in PROSPERO, the review was conducted in August 2024 across various databases. Eligible in vivo studies were analysed for their assessment of isotretinoin's effects on craniomaxillofacial bone.
Med Oncol
September 2025
Venom and Biotherapeutics Molecules Laboratory, Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran, Tehran, Iran.
Neuropeptide Y (NPY) and the voltage-gated potassium channel Kv1.3 are closely associated with breast cancer progression and apoptosis regulation, respectively. NPY receptors (NPYRs), which are overexpressed in breast tumors, contribute to tumor growth, migration, and angiogenesis.
View Article and Find Full Text PDFMol Biol Rep
September 2025
Department of Pharmacology, Govt. College of Pharmacy, Rohru, Shimla, Himachal Pradesh, 171207, India.
Alzheimer's disease (AD) is the most common, complex, and untreatable form of dementia which is characterized by severe cognitive, motor, neuropsychiatric, and behavioural impairments. These symptoms severely reduce the quality of life for patients and impose a significant burden on caregivers. The existing therapies offer only symptomatic relief without addressing the underlying silent pathological progression.
View Article and Find Full Text PDFDiabetologia
September 2025
Center for Clinical Metabolic Research, Gentofte Hospital, University of Copenhagen, Hellerup, Denmark.
Aims/hypothesis: Alpha cell dysregulation is an integral part of type 2 diabetes pathophysiology, increasing fasting as well as postprandial glucose concentrations. Alpha cell dysregulation occurs in tandem with the development of insulin resistance and changes in beta cell function. Our aim was to investigate, using mathematical modelling, the role of alpha cell dysregulation in beta cell compensatory insulin secretion and subsequent failure in the progression from normoglycaemia to type 2 diabetes defined by ADA criteria.
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