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The pyrethroid insecticide permethrin confers hepatotoxicity through DNA damage and mitochondria-associated apoptosis induction in rat: Palliative benefits of Fumaria officinalis.
J Biochem Mol Toxicol
October 2022
Laboratory of Animal Eco-Physiology, Faculty of Sciences of Sfax, University of Sfax, Sfax, Tunisia.
Permethrin (PER) is a pyrethroid pesticide that is extensively used as an insecticide in world because of its high activity and its low mammalian toxicity. The current study was conducted to investigate the protective action of Fumaria officinalis against PER-induced liver injury in male rats. However, HPLC-DAD showed the richness of 6 components in F.
View Article and Find Full Text PDFEvaluation of the human hazard of the liver and lung tumors in mice treated with permethrin based on mode of action.
Crit Rev Toxicol
January 2022
Department of Pathology and Microbiology, Havlik-Wall Professor of Oncology, University of Nebraska Medical Center, 983135 Nebraska Medical Center, Omaha, NE, USA.
The non-genotoxic synthetic pyrethroid insecticide permethrin produced hepatocellular adenomas and bronchiolo-alveolar adenomas in female CD-1 mice, but not in male CD-1 mice or in female or male Wistar rats. Studies were performed to evaluate possible modes of action (MOAs) for permethrin-induced female CD-1 mouse liver and lung tumor formation. The MOA for liver tumor formation by permethrin involves activation of the peroxisome proliferator-activated receptor alpha (PPARα), increased hepatocellular proliferation, development of altered hepatic foci, and ultimately liver tumors.
View Article and Find Full Text PDFInduction of distinct neuroinflammatory markers and gut dysbiosis by differential pyridostigmine bromide dosing in a chronic mouse model of GWI showing persistent exercise fatigue and cognitive impairment.
Life Sci
January 2022
Department of Molecular, Cell and Systems Biology, University of California, Riverside, CA, USA. Electronic address:
Aims: To characterize neuroinflammatory and gut dysbiosis signatures that accompany exaggerated exercise fatigue and cognitive/mood deficits in a mouse model of Gulf War Illness (GWI).
Methods: Adult male C57Bl/6N mice were exposed for 28 d (5 d/wk) to pyridostigmine bromide (P.O.
Delayed treatment with the immunotherapeutic LNFPIII ameliorates multiple neurological deficits in a pesticide-nerve agent prophylactic mouse model of Gulf War Illness.
Neurotoxicol Teratol
January 2022
Department of Physiology and Pharmacology, University of Georgia, Athens, GA, United States; Neuroscience Program, University of Georgia, Athens, GA, United States; Interdisciplinary Toxicology Program, University of Georgia, Athens, GA, United States. Electronic address:
Residual effects of the 1990-1991 Gulf War (GW) still plague veterans 30 years later as Gulf War Illness (GWI). Thought to stem mostly from deployment-related chemical overexposures, GWI is a disease with multiple neurological symptoms with likely immunological underpinnings. Currently, GWI remains untreatable, and the long-term neurological disease manifestation is not characterized fully.
View Article and Find Full Text PDFVagus Nerve Stimulation Ameliorates Cognitive Impairment and Increased Hippocampal Astrocytes in a Mouse Model of Gulf War Illness.
Neurosci Insights
May 2021
Department of Neuroscience and Experimental Therapeutics, Texas A&M University, Bryan, TX, USA.
Gulf war illness (GWI), is a chronic multi-symptom illness that has impacted approximately one-third of the veterans who served in the 1990 to 1991 Gulf War. GWI symptoms include cognitive impairments (eg, memory and concentration problems), headaches, migraines, fatigue, gastrointestinal and respiratory issues, as well as emotional deficits. The exposure to neurological chemicals such as the anti-nerve gas drug, pyridostigmine bromide (PB), and the insecticide permethrin (PER), may contribute to the etiologically related factors of GWI.
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