scholarly journals A fish oil-rich diet leads to lower adiposity and serum triglycerides but increases liver lipid peroxidation in fructose-fed rats

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Gabriel Perri Esteves ◽  
Camila Sanches Manca ◽  
Hellen Paraguassú Veida-Silva ◽  
Paula Payão Ovidio ◽  
Héric Holland ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fish Oil ◽  
Liver Lipid ◽  
Serum Triglycerides ◽  
Liver Lipid Peroxidation

Dietary trans-resveratrol bioavailability and effect on CCl4-induced liver lipid peroxidation

2009 ◽  
Vol 24 (4) ◽  
pp. 618-622 ◽  
Author(s):  
Paola Vitaglione ◽  
Barbara Ottanelli ◽  
Stefano Milani ◽  
Filomena Morisco ◽  
Nicola Caporaso ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Liver Lipid ◽  
Liver Lipid Peroxidation

Brain and liver lipid peroxidation levels following acute and short-term lindane administration in the rat

1994 ◽  
Vol 74 (1) ◽  
pp. 61-68 ◽  
Author(s):  
Ana Carolina M. Arisi ◽  
Simizu Kiyoko ◽  
Kogake Marisa ◽  
Afonso C.D. Barny ◽  
Marcia A.S. Silva ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Liver Lipid ◽  
Short Term ◽  
Liver Lipid Peroxidation

Biochemical evidence for free radicalinduced lipid peroxidation as a mechanism for subchronic toxicity of malathion in blood and liver of rats

2003 ◽  
Vol 22 (4) ◽  
pp. 205-211 ◽  
Author(s):  
Maryam Akhgari ◽  
Mohammad Abdollahi ◽  
Abbas Kebryaeezadeh ◽  
Ruhollah Hosseini ◽  
Omid Sabzevari
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Free Radicals ◽  
Oxygen Free Radicals ◽  
Organophosphorus Compounds ◽  
Liver Lipid ◽  
Subchronic Toxicity ◽  
Male Wistar Rats ◽  
Liver Lipid Peroxidation ◽  
Different Doses

Organophosphorus compounds may induce oxidative stress leading to generation of free radicals and alterations in antioxidant and scavengers of oxygen free radicals (OFRs). The effect of subchronic exposure to malathion in the production of oxidative stress was evaluated in male Wistar rats. Administration of malathion (100, 316, 1000, 1500 ppm) for 4 weeks increased catalase (CAT), superoxide dismutase (SOD) activities as well as malondialdehyde (MDA) concentration in red blood cells (RBC) and liver. However, acetylcholinesterase (AChE) and cholinesterase (ChE) activities were decreased in these samples. The increase in RBC and liver lipid peroxidation correlated well with the inhibition in RBC AChE and liver ChE activities. Elevation of MDA concentrations and increased activities of CAT and SOD showed significant correlations in both RBC and liver samples when different doses of malathion were used. The results of the present study suggest the usefulness of RBC AChE measurement as a good biomarker in the estimation of malathion-induced oxidative stress affecting blood and liver.

Effect of a Urinary Preparation on Liver Injury by Short-term Carbon Tetrachloride Treatment in Rats

1999 ◽  
Vol 27 (02) ◽  
pp. 241-250 ◽  
Author(s):  
Tung-Yuan Lai ◽  
Yueh-Wern Wu ◽  
Wen-Chuan Lin
Keyword(s):  
Lipid Peroxidation ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Catalase Activity ◽  
Liver Lipid ◽  
Oxygen Metabolism ◽  
Short Term ◽  
Active Oxygen Metabolism ◽  
Serum Biochemical ◽  
Liver Lipid Peroxidation

The hepatoprotective effect of a preparation of human urine (PHU) was assessed against short-term carbon tetrachloride (CCl4) treatment in rats. Significant prevention of liver injury by PHU was found after CCl4 treatment, judging by the changes of serum biochemical parameters, and hepatic protein and triglyceride contents. The increased liver lipid peroxidation, and decreased liver vitamin C concentrations observed after CCl4 treatment were significantly prevented by PHU administration. The increase in liver glutathione (GSH) contents observed after CCl4 treatment was further increased by PHU treatment. Liver catalase activity decreased after CCl4 treatment, while liver superoxide dismutase and GSH-peroxidase activities did not change. PHU administration further inhibited the decrease in liver catalase activity after CCl4 treatment. These results indicate that PHU administration can prevent liver injury induced by CCl4 in rats by inhibiting enhanced lipid peroxidation and by improving disrupted active oxygen metabolism in the injured liver.

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