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APOB — SOD2

Text-mined interactions from Literome

Zhao et al., Atherosclerosis 2005 (Arteriosclerosis) : Gly-LDL caused less increases in SOD , GPx or catalase activity, but more evident changes in GR activity and H ( 2 ) O ( 2 ) release compared to oxLDL or LDL
Wang et al., J Appl Physiol 2006 : This experiment obtained the following findings : 1 ) ox-LDL increased monocyte ROS production and was accompanied by decreased c-SOD and m-SOD activities, as well as t-GSH and r-GSH contents, whereas treating monocytes with diphenyleneiodonium ( DPI ) ( a NADPH oxidase inhibitor ) or rotenone/2-thenoyltrifluoroacetone ( TTFA ) ( mitochondrial complex I/II inhibitors ) hindered ox-LDL induced monocyte ROS production ; 2 ) production of ROS and reduction of m-SOD activity and r-GSH content in monocyte by ox-LDL were enhanced by heavy exercise and depressed by mild and moderate exercise ; and 3 ) heavy exercise augmented the inhibition of ox-LDL induced monocyte ROS production by DPI and rotenone/TTFA, whereas these DPI- and rotenone/TTFA mediated monocyte ROS productions were unchanged in response to mild and moderate exercise
Bao et al., J Cardiovasc Pharmacol 2006 : Besides, it was observed that ox-LDL triggered superoxide production and suppressed the superoxide dismutase activity, both of which could be prevented by FSBT pretreatment
Uchiyama et al., J Biol Chem 2006 (Hepatitis) : CuZn-SOD deficiency causes ApoB degradation and induces hepatic lipid accumulation by impaired lipoprotein secretion in mice
Verreth et al., Br J Pharmacol 2007 (Atherosclerosis...) : Rosuvastatin restores superoxide dismutase expression and inhibits accumulation of oxidized LDL in the aortic arch of obese dyslipidemic mice
Rankin et al., J Lipid Res 1991 : SOD had a greater inhibitory effect on the modification of LDL by U937 cells and fibroblasts ( 32 % and 64 %, respectively ) but again LO inhibitors had a much greater effect ( 79 to 100 % inhibition )
Kumar et al., Indian J Biochem Biophys 2010 (Diabetes Mellitus, Experimental) : The decrease of lipids and apoprotein levels of VLDL and LDL were followed by stimulation of plasma post-heparin lipolytic activity and lecithin cholesterol acyltransferase as well as hepatic superoxide dismutase and catalase activities
McNally et al., J Immunol 1990 : In this study, the requirement for lipoxygenase activity is shown, in that 1 ) inhibitors of lipoxygenase prevent the alteration of LDL, 2 ) copper ( II ) ( 3,5-diisopropylsalicylic acid ), an agent shown to enhance lipoxygenase activity in a cell-free system, similarly enhances monocyte mediated LDL alteration, and 3 ) the ( 3,5-diisopropylsalicylic acid ) -enhanced monocyte mediated modification of LDL can be completely blocked by inhibitors of lipoxygenase or by superoxide dismutase
Xu et al., Wei Sheng Yan Jiu 2011 (Hyperlipidemias) : In comparison with high fat diet model group, serum TC, TG, LDL-C and MDA were decreased but HDL-C and SOD were increased in lycopene groups
Kinscherf et al., FASEB J 1997 (Arteriosclerosis...) : Induction of mitochondrial manganese superoxide dismutase in macrophages by oxidized LDL : its relevance in atherosclerosis of humans and heritable hyperlipidemic rabbits