In order to explore the influences of iron overload on lipid peroxidation of rats and the inhibiting effects of antioxidant vitamins such as vitamin E and beta-carotene on the influences induced by iron overload, eighty male Wistar rats were randomly divided into 8 groups according to the weight. The diets of the former 4 groups differed only in iron concentration (50, 200, 350 or 500 mg/kg diet). The diet of the latter 4 groups were consistent with the former 4 groups respectively, but complemented with vitamin E(100 mg/kg diet) and beta-carotene (25 mg/kg.BW) at the same time. After Eight weeks, the levels of serum iron, blood lipid including total cholesterol TC, triglyceride TG, high density lipoprotein HDL, low density lipoprotein LDL, vitamin E, vitamin A, serum malondialdehyde (MDA) and oxidized low density lipoprotein (OX-LDL), the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were determined. Results showed that the iron overload increased the levels of MDA, OX-LDL and LDL in serum, especially in the group of rat with 500 mg/kg diet. The activity of GSH-Px increased irritably and the contents of Vitamin E and Vitamin A decreased significantly. Complementing antioxidant vitamins decreased the levels of MDA, OX-LDL and LDL and increased HDL and the activity of GSH-Px decreased compared with the corresponding iron overload groups. It was concluded that iron overload could promote lipid peroxidation reaction especially in 10 folds of physiologic dose and the activities of antioxidant enzymes increased at the same time to keep the body homeostasis. Antioxidant vitamins may play a role through non-enzymatic reactive system to inhibit the above changes.
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Biology (Basel)
January 2025
Key Laboratory of Animal Physiology and Biochemistry, Ministry of Agriculture and Rural Affairs, College of Veterinary Medicine, Nanjing Agricultural University, Nanjing 210095, China.
Iron is a trace element that is indispensable for the growth and development of animals. Excessive iron supplementation may lead to iron overload and elevated reactive oxygen species (ROS) production in animals, causing cellular damage. Nevertheless, the precise mechanism by which iron overload causes cell injury remains to be fully elucidated.
View Article and Find Full Text PDFACS Appl Mater Interfaces
January 2025
Department of Neurosurgery, Guizhou Provincial People's Hospital, Guiyang 550000, China.
Spontaneous intracerebral hemorrhagic stroke (ICH) is a highly aggressive disease, with a high incidence and mortality rate. Iron deposition following ICH leads to oxidative damage and motor dysfunction, significantly impacting the overall quality of life for those affected. Here, a polyphenolic nanomedicine, catechin-based polyphenol nanoparticles surface-modified by thiol-terminated poly(ethylene glycol) (CNPs@PEG), was developed through the oxidative polymerization and self-assembly of catechin, a natural compound in tea.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Orthopedics, The Second Affiliated Hospital of Anhui Medical University, Hefei, 230601, China.
Excessive iron deposition can lead to ferroptosis, a form of iron-dependent cell death detrimental to neuronal survival. Microglia have been identified as having a high capacity for iron deposition, yet it remains unclear whether microglia undergo ferroptosis while phagocytosing excessive amounts of iron after spinal cord injury (SCI). Here, we observed scattered iron around the epicenter of the injured spinal cord at 7 days post-injury (dpi) in mice, which then accumulated in the lesion core at 14 dpi.
View Article and Find Full Text PDFJ Control Release
January 2025
State Key Laboratory of Quality Research in Chinese Medicine, Institute of Chinese Medical Sciences, University of Macau, Macau SAR 999078, China. Electronic address:
Nanomedicine-driven ferroptosis has emerged as a promising tumor treatment strategy through delivering exogenous iron and aggravating the lethal accumulation of lipid peroxides (LPO). However, the compensatory mechanisms of ferroptosis defense systems in cancer cells compromise the therapeutic efficacy and lead to potential side effects. Herein, a highly effective ferroptotic nano-amplifier is designed to synergistically promote ferroptosis via increasing intracellular labile iron, exacerbating lipid peroxidation and overcoming the defense system.
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