Evaluation of liver lipid peroxidation and antioxidant profile in broiler chicken fed with mixture of T-2 toxin and endosulfan

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.

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

The American Journal of Chinese Medicine ◽

10.1142/s0192415x99000276 ◽

1999 ◽

Vol 27 (02) ◽

pp. 241-250 ◽

Cited By ~ 4

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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Reduced Liver Lipid Peroxidation in Subcellular Fractions Is Associated with a Hypometabolic State in Rats with Portacaval Anastomosis

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/4565238 ◽

2019 ◽

Vol 2019 ◽

pp. 1-13 ◽

Cited By ~ 2

Author(s):

Olivia Vázquez-Martínez ◽

Héctor Valente-Godínez ◽

Andrés Quintanar-Stephano ◽

Deisy Gasca-Martínez ◽

Mayra L. López-Cervantes ◽

...

Keyword(s):

Lipid Peroxidation ◽

Liver Lipid ◽

Liver Homogenate ◽

Calcium Content ◽

Portacaval Anastomosis ◽

Serum Aspartate Aminotransferase ◽

Significant Attenuation ◽

Hypometabolic State ◽

Altered Blood ◽

Liver Lipid Peroxidation

A surgical connection between portal and inferior cava veins was performed to generate an experimental model of high circulating ammonium and hepatic hypofunctioning. After 13 weeks of portacaval anastomosis (PCA), hyperammonemia and shrinkage in the liver were observed. Low glycemic levels accompanied by elevated levels of serum alanine aminotransferase were recorded. However, the activity of serum aspartate aminotransferase was reduced, without change in circulating urea. Histological and ultrastructural observations revealed ongoing vascularization and alterations in the hepatocyte nucleus (reduced diameter with indentations), fewer mitochondria, and numerous ribosomes in the endoplasmic reticulum. High activity of hepatic caspase-3 suggested apoptosis. PCA promoted a marked reduction in lipid peroxidation determined by TBARs in liver homogenate but specially in the mitochondrial and microsomal fractions. The reduced lipoperoxidative activity was also detected in assays supplemented with Fe2+. Only discreet changes were observed in conjugated dienes. Fluorescent probes showed significant attenuation in mitochondrial membrane potential, reactive oxygen species (ROS), and calcium content. Rats with PCA also showed reduced food intake and decreased energy expenditure through indirect calorimetry by measuring oxygen consumption with an open-flow respirometric system. We conclude that experimental PCA promotes an angiogenic state in the liver to confront the altered blood flow by reducing the prooxidant reactions associated with lower metabolic rate, along with significant reduction of mitochondrial content, but without a clear hepatic dysfunction.

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