Paper
Dose-dependent biochemical changes in rat central nervous system after 12-week exposure to 1-bromopropane.
Published Mar 1, 2003 · Hailan Wang, G. Ichihara, Hidenori Ito
Neurotoxicology
Q2 SJR score
49
Citations
1
Influential Citations
Abstract
Abstract hidden due to publisher request; this does not indicate any issues with the research. Click the full text link above to read the abstract and view the original source.
Study Snapshot
Long-term exposure to 1-bromopropane in rats leads to dose-dependent biochemical changes in the central nervous system, suggesting potential neurotoxic mechanisms.
PopulationOlder adults (50-71 years)
Sample size24
MethodsObservational
OutcomesBody Mass Index projections
ResultsSocial networks mitigate obesity in older groups.
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References
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Citations
1-Bromopropane-induced apoptosis in OVCAR-3 cells via oxidative stress and inactivation of Nrf2
1-BP induces oxidative stress and apoptosis in OVCAR-3 cells through inactivation of Nrf2 signaling, with vitamin C alleviating this toxicity by inhibiting caspase activity.
2020·8citations·Guangtao Yang et al.·Toxicology and Industrial Health
Toxicology and Industrial Health
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Toxic peripheral neuropathies are caused by various agents, primarily through modifications, compromised energy or protein biosynthesis, oxidative injury, and disruption of ionic gradients across membranes.
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Identification of DNA and glutathione adducts in male Sprague–Dawley rats exposed to 1-bromopropane
1-BP exposure in male Sprague-Dawley rats leads to DNA and glutathione adduct formation, which may serve as useful markers for exposure assessment.
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Effect of 4‐week inhalation exposure to 1‐bromopropane on blood pressure in rats
Subacute (4-week) inhalation exposure to 1bromopropane increases blood pressure in rats, with this cardiovascular toxic effect partly due to increased oxidative stress mediated through activation of the NADPH oxidase pathway.
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Preliminary characterization of a murine model for 1-bromopropane neurotoxicity: Role of cytochrome P450.
Controlling hepatic P450 activity with 1-aminobenzotriazole (1-ABT) allows mice to experience higher concentrations of 1-bromopropane neurotoxicity, potentially providing better models for 1-bromopropane-induced neurotoxicity.
2016·12citations·Cai Zong et al.·Toxicology letters
Toxicology letters
Identify Melatonin as a Novel Therapeutic Reagent in the Treatment of 1-Bromopropane(1-BP) Intoxication
Melatonin treatment reduces 1-BP-induced CNS toxicity and improves memory and spatial learning abilities in rats by restoring antioxidant balance and redox homeostasis.
2016·9citations·Yongpeng Xu et al.·Medicine
Medicine
Neurotoxicity associated with exposure to 1-bromopropane in golf-club cleansing workers
Occupational exposure to 1-BP can cause neurotoxicity, including peripheral neuropathy and adverse CNS effects, with urine AcPrCys potentially being a specific biomarker for exposure.
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Clinical Toxicology
Physiologically based pharmacokinetic modeling for 1-bromopropane in F344 rats using gas uptake inhalation experiments.
The PBPK model for 1-bromopropane accurately simulates its closed chamber concentration in rats, helping to understand its metabolism and potential risks in workers.
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