Tissues changes in FA metabolism can occur quite rapidly in response to ischemia and may require immediate microwave fixation to determine basal concentrations. The present study aimed to quantify the effects of immediate no-flow ischemia on concentrations of individual nonesterified FA (NEFA) and acyl-CoA species in the rat heart. Male CDF 344 rats were anesthetized and decapitated either 5 min prior to being microwaved (5.5 kW, 3.4 s, twice) to produce ischemia or microwaved prior to decapitation (nonischemic). Hearts were then removed and used to measure the concentrations of acyl-CoA species and FA in several lipid classes. The ischemic heart total NEFA concentration was significantly lower than that in the nonischemic heart (11.9 vs. 19.0 nmol/g). Several individual NEFA concentrations were decreased by 31-85%. Ischemic heart total long-chain acyl-CoA concentrations (21.0 nmol/g) were significantly higher than those in nonischemic hearts (11.4 nmol/g). Increased concentrations of individual acyl-CoA species occurred in palmitoyl-CoA, stearoyl-CoA, oleoyl-CoA, and linoleoyl-CoA. Concentrations of short-chain acetyl-CoA and beta-hydroxy-beta-methylglutaryl-CoA were also two- to three-fold higher in ischemic hearts than in nonischemic hearts. The FA concentration in TG and phospholipids generally did not differ between the groups. Decreases in concentrations of individual FA and increases in acyl-CoA species during no-flow ischemia occur very rapidly within the heart. Although it is not clear how these alterations contribute to the pathogenesis of ischemia, it is evident that future studies attempting to quantify basal levels of these metabolites could use microwave fixation.
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http://dx.doi.org/10.1007/s11745-005-1479-9 | DOI Listing |
Nan Fang Yi Ke Da Xue Xue Bao
December 2024
Department of Histology and Embryology, School of Basic Medical Sciences, Xinjiang Medical University, Urumqi 830000, China.
Objectives: To investigate the inhibitory effect of FER-1 on methylglyoxal-induced ferroptosis in cultured mouse alveolar macrophages.
Methods: MH-S cells derived from mouse alveolar macrophages treated with 90 μg/mL methylglyoxal, 10 μmol/mL FER-1MG+FER-1, or both were examined for intracellular reactive oxygen species (ROS), malondialdehyde (MDA) and ferrous ion (Fe) levels and changes in mitochondrial membrane potential. Western blotting was performed to detect the protein expression levels of glutathione peroxidase 4 (GPX4) and long-chain acyl-CoA synthase 4 (ACSL4).
Ecotoxicol Environ Saf
December 2024
College of Basic Medicine and Forensic Medicine, Henan University of Science and Technology, Luoyang, China. Electronic address:
Recent studies demonstrate that lipid peroxidation-induced ferroptosis participates in 2,2',4,4'-tetrabromodiphenyl ether (BDE-47)-evoked neurotoxicity and cognitive dysfunction. Melatonin has been indicated to confer neuroprotection against brain diseases via its potent anti-ferroptotic effects. Therefore, this study aims to explore whether melatonin can mitigate BDE-47-elicited cognitive impairment via suppressing ferroptosis, and further delineate the underlying mechanisms.
View Article and Find Full Text PDFZhen Ci Yan Jiu
December 2024
School of Acupuncture-moxibustion and Tuina, Anhui University of Chinese Medicine, Hefei 230038, China.
Am J Transl Res
November 2024
Department of Hepatic Surgery IV, The Eastern Hepatobiliary Surgery Hospital, Third Affiliated Hospital of Naval Medical University Shanghai 200438, The People's Republic of China.
Background: The mechanism of ferroptosis is primarily driven by the iron-dependent lethal accumulation of membrane lipid peroxidation. Bavachin has been found to exacerbate lipid peroxidation in cancer cells; however, whether it hinders hepatocellular carcinoma (HCC) progression by way of ferroptosis remains unknown.
Methods: Cell counting kit-8 (CCK-8) assay was used to measure the effect of Bavachin on the viability of HCC cells, so as to determine the appropriate drug concentration for subsequent experiments.
J Lipid Res
December 2024
Department of Medicine, Division of Metabolism, Endocrinology and Nutrition, University of Washington, Seattle WA 98109; UW Medicine Diabetes Institute, University of Washington, Seattle WA 98109; Department of Laboratory Medicine and Pathology, University of Washington, Seattle WA 98109. Electronic address:
Long-chain acyl-CoA synthetase 1 (ACSL1) catalyzes the conversion of long-chain fatty acids to acyl-CoAs. ACSL1 is required for β-oxidation in tissues that rely on fatty acids as fuel, but no consensus exists on why ACSL1 is induced by inflammatory mediators in immune cells. We used a comprehensive and unbiased approach to investigate the role of ACSL1 induction by interferon type I (IFN-I) in myeloid cells in vitro and in a mouse model of IFN-I overproduction.
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