UVA-induced lipid peroxidation in cultured human skin fibroblasts, as measured by the release in the supernatant of thiobarbituric acid-reactive substances, is found to be linear with increasing irradiation dose (up to about 250 kJ m(-2)). Concomitantly, within this dose range catalase is strongly inactivated by UVA radiation according to an exponential process (k≈0.01 kJ(-1) m(2)). This suggests that catalase is not involved in modulating the peroxidation process. Inactivation of catalase by 3-amino-1,2,4-triazole can be efficiently achieved prior to irradiation. This inactivation has no consequence on the extent of peroxidation triggered by subsequent exposure to UVA radiation. It may be therefore strongly suggested that catalase is not, via H2O2 removal, a key enzyme in the cellular defence equipment towards UV A-peroxidative stress. An alternative interpretation may be formulated which supports the view that H2O2 produced upon exposure to UVA has no or very little role in triggering the lipid peroxidation process.
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http://dx.doi.org/10.1080/13510002.1995.11746967 | DOI Listing |
Med Oncol
January 2025
Laboratory of Molecular Toxicology, Faculty of Nature and Life Sciences, University of Jijel, 18000, Jijel, Algeria.
The current study aimed to assess the preventive effects of aqueous leaf extract of Pistacia lentiscus (ALEPL) against Oxaliplatin (OXA)-induced DNA damage, hepatic injury, and oxidative stress. The in vitro cytotoxic and genotoxic effects of OXA and ALEPL on HCT116 colon cancer cells were evaluated using the MTT (Tetrazolium salt reduction) assay and comet assay. The in vivo study involved 24 female NMRI (Naval Medical Research Institute) mice that were equally divided into four groups as follows: Control group, ALEPL-treated group (100 mg/kg), OXA-treated group (7 mg/kg), and ALEPL-treated group (100mg/kg) + OXA (7mg/kg).
View Article and Find Full Text PDFCell Death Dis
January 2025
Faculty of Medicine, Institute of Biochemistry I, Goethe University Frankfurt, Frankfurt, Germany.
Arachidonate 15-lipoxygenase type B (ALOX15B) peroxidises polyunsaturated fatty acids to their corresponding fatty acid hydroperoxides, which are subsequently reduced into hydroxy-fatty acids. A dysregulated abundance of these biological lipid mediators has been reported in the skin and blood of psoriatic compared to healthy individuals. RNAscope and immunohistochemistry revealed increased ALOX15B expression in lesional psoriasis samples.
View Article and Find Full Text PDFJ Appl Toxicol
January 2025
Department of Zoology, Guru Nanak Dev University, Amritsar, India.
This study aimed to provide insights into the hepatorenal toxicity induced by erythrosine, a synthetic red dye commonly used in food and pharmaceuticals, which has raised concerns over its potential health risks. Twenty-four rats were randomly divided into four groups (n = 6). The first group was the control group and the other group received one of three doses of erythrosine based on acceptable daily intake (¼ ADI, ½ ADI, and ADI, 0.
View Article and Find Full Text PDFJ Physiol Sci
January 2025
Department of Critical Care Medicine, The Third People's Hospital of Qingdao, No. 29 Yongping Road, Licang District, 266000, Qingdao, Shandong, China. Electronic address:
Background: Sepsis-induced acute lung injury (ALI) accounts for about 40% of ALI, accompanied by alveolar epithelial injury. The study aimed to reveal the role of circular RNA_0114428 (circ_0114428) in sepsis-induced ALI.
Methods: Human pulmonary alveolar epithelial cells (HPAEpiCs) were treated with lipopolysaccharide (LPS) to mimic a sepsis-induced ALI cell model.
J 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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