Oxidant injury to hepatic mitochondrial lipids in rats with dietary copper overload

Sokol, Ronald J.; Devereaux, Michael W.; Mierau, Gary W.; Hambidge, K. Michael; Shikes, Robert H.

doi:10.1016/0016-5085(90)90627-d

Cited by 127 publications

(68 citation statements)

References 37 publications

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“…The crude mitochondrial pellet was further purified by sucrosepercoll gradient centrifugation. 68 The pellet was resuspended in 2 ml of homogenate buffer, and 1 ml of the resuspended pellet was carefully layered onto a 35-ml self-generating gradient containing 0.25 M sucrose, 1 mM EGTA and percoll (Pharmacia Fine Chemicals, Piscataway, NJ, USA) (75 : 25, v/v). The mitochondria were purified by centrifugation at 43 0006g for 30 min at 48C using a Beckman Ti60 rotor and a Beckman ultracentrifuge model L8-55 (Beckman Instruments, Inc., Schaumburg, IL, USA).…”

Section: Isolation Of Mitochondriamentioning

confidence: 99%

Ursodeoxycholic acid prevents cytochrome c release in apoptosis by inhibiting mitochondrial membrane depolarization and channel formation

et al. 1999

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The hydrophilic bile salt ursodeoxycholic acid (UDCA) is a potent inhibitor of apoptosis. In this paper, we further characterize the mechanism by which UDCA inhibits apoptosis induced by deoxycholic acid, okadaic acid and transforming growth factor b1 in primary rat hepatocytes. Our data indicate that coincubation of cells with UDCA and each of the apoptosis-inducing agents was associated with an approximately 80% inhibition of nuclear fragmentation (P50.001). Moreover, UDCA prevented mitochondrial release of cytochrome c into the cytoplasm by 70 ± 75% (P50.001), thereby, inhibiting subsequent activation of DEVD-specific caspases and cleavage of poly(ADP-ribose) polymerase. Each of the apoptosis-inducing agents decreased mitochondrial transmembrane potential and increased mitochondrial-associated Bax protein levels. Coincubation with UDCA was associated with significant inhibition of these mitochondrial membrane alterations. The results suggest that the mechanism by which UDCA inhibits apoptosis involves an interplay of events in which both depolarization and channel-forming activity of the mitochondrial membrane are inhibited.

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Section: Isolation Of Mitochondriamentioning

confidence: 99%

Ursodeoxycholic acid prevents cytochrome c release in apoptosis by inhibiting mitochondrial membrane depolarization and channel formation

et al. 1999

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“…3 ) Although it has not been conclusively determined whether lipid peroxidation is involved in hepatic injury, mitochondrial lipid peroxidation in animal models of liver injury has been associated with a wide range of functional consequences that may impair cellular energy metabolism and viability.4) In fact, Sokol et al 5 ) have shown that free radical stress occurred after bile duct ligation in rats, and may result in mitochondrial lipid peroxidation. They have also shown that diets high in lipid and deficient in vitamin E may increase the free radical damage to hepatic mitochondria.…”

Section: Bifidobacterium Longum (B Longum) Lactobacillus Acidophilumentioning

confidence: 99%

Effect of Milk Whey and Its Fermentation Products by Lactic Acid Bacteria on Mitochondrial Lipid Peroxide and Hepatic Injury in Bile Duct-ligated Rats

Zommara¹,

Takagi²,

Sakono³

et al. 1994

Bioscience, Biotechnology, and Biochemistry

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“…This has been manifested as increased production of pentane and hepatic malondialdehyde when liver homogenates or hepatocytes are exposed to ionic copper. Moreover, dietary copper overload in rats resulted in in vivo peroxidation of mitochondrial membrane lipids demontstrated by increased concentrations of conjugated dienes and thiobarbituric acid-reacting substances (TBARS) [25,58]. Copper-catalyzed lipid peroxidation also appears to underlie the alterations in hepatocyte lysosomes in copper-loaded rats [45].…”

Section: Copper As Active Ingredient Of Pesticides and Oxidative Stressmentioning

confidence: 99%

“…Cu-overloaded rats exhibited oxidative injury including decreased levels of hepatic GSH and α-tocopherol, increased levels of mitochondrial lipid peroxidation products, decreases in state 3 respiration of mitochondria and the respiratory control ratio in hepatic mitochondria, and decreased complex IV (cytochrome c oxidase) activity [58].…”

Section: Copper As Active Ingredient Of Pesticides and Oxidative Stressmentioning

confidence: 99%

Copper and Copper-Containing Pesticides: Metabolism, Toxicity and Oxidative Stress

Husak

2015

jpnu

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Abstract. The purpose of this paper is to provide a brief review of the current knowledge regarding metabolism and toxicity of copper and copper-based pesticides in living organisms. Copper is an essential trace element in all living organisms (bacteria, fungi, plants, and animals), because it participates in different metabolic processes and maintain functions of organisms. The transport and metabolism of copper in living organisms is currently the subject of many studies. Copper is absorbed, transported, distributed, stored, and excreted in the body via the complex of homeostatic processes, which provide organisms with a needed constant level of this micronutrient and avoid excessive amounts. Many aspects of copper homeostasis were studied at the molecular level. Copper based-pesticides, in particularly fungicides, bacteriocides and herbicides, are widely used in agricultural practice throughout the world. Copper is an integral part of antioxidant enzymes, particularly copper-zinc superoxide dismutase (Cu,Zn-SOD), and plays prominent roles in iron homeostasis. On the other hand, excess of copper in organism has deleterious effect, because it stimulates free radical production in the cell, induces lipid peroxidation, and disturbs the total antioxidant capacity of the body. The mechanisms of copper toxicity are discussed in this review also.

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Oxidant injury to hepatic mitochondrial lipids in rats with dietary copper overload

Cited by 127 publications

References 37 publications

Ursodeoxycholic acid prevents cytochrome c release in apoptosis by inhibiting mitochondrial membrane depolarization and channel formation

Ursodeoxycholic acid prevents cytochrome c release in apoptosis by inhibiting mitochondrial membrane depolarization and channel formation

Effect of Milk Whey and Its Fermentation Products by Lactic Acid Bacteria on Mitochondrial Lipid Peroxide and Hepatic Injury in Bile Duct-ligated Rats

Copper and Copper-Containing Pesticides: Metabolism, Toxicity and Oxidative Stress

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