Mechanism of induction of oxidative stress in liver mitochondria by low concentrations of tert-butyl hydroperoxide

Sargassum species have been reported to be a source of phytochemicals, with a wide range of biological activities. In this study, we evaluated the hepatoprotective effect of a meroterpenoid-rich fraction of the ethanolic extract from Sargassum serratifolium (MES) against tert-butyl hydroperoxide (t-BHP)-treated HepG2 cells. Treatment with MES recovered the cell viability from the t-BHP-induced oxidative damage in a dose-dependent manner. It suppressed the reactive oxygen species production, lipid peroxidation, and glutathione depletion in the t-BHP-treated HepG2 cells. The activity of the antioxidants induced by t-BHP, including superoxide dismutase (SOD) and catalase, was reduced by the MES treatment. Moreover, it increased the nuclear translocation of nuclear factor erythroid 2-related factor 2, leading to the enhanced activity of glutathione S transferase, and the increased production of heme oxygenase-1 and NAD(P)H:quinine oxidoreductase 1 in t-BHP-treated HepG2 cells. These results demonstrate that the antioxidant activity of MES substituted the activity of the SOD and catalase, and induced the production of detoxifying enzymes, indicating that MES might be used as a hepatoprotectant against t-BHP-induced oxidative stress.

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Pyridine-nucleotide oxidation, Ca2+ cycling and membrane damage during tert-butyl hydroperoxide metabolism by rat-liver mitochondria

European Journal of Biochemistry ◽

10.1111/j.1432-1033.1984.tb08058.x ◽

1984 ◽

Vol 140 (1) ◽

pp. 1-6 ◽

Cited By ~ 114

Author(s):

Giorgio BELLOMO ◽

Anna MARTINO ◽

Plinio RICHELMI ◽

Gregory A. MOORE ◽

Sarah A. JEWELL ◽

...

Keyword(s):

Rat Liver ◽

Membrane Damage ◽

Pyridine Nucleotide ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Butyl Hydroperoxide ◽

Tert Butyl ◽

Tert Butyl Hydroperoxide ◽

Pyridine Nucleotide Oxidation ◽

Hydroperoxide Metabolism

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An aqueous extract of Rubus chingii fruits protects primary rat hepatocytes against tert-butyl hydroperoxide induced oxidative stress

Life Sciences ◽

10.1016/s0024-3205(02)02239-7 ◽

2002 ◽

Vol 72 (3) ◽

pp. 329-338 ◽

Cited By ~ 29

Author(s):

Ming-Hon Yau ◽

Chun-Tao Che ◽

Song-Ming Liang ◽

Yun-Cheung Kong ◽

Wing-Ping Fong

Keyword(s):

Oxidative Stress ◽

Aqueous Extract ◽

Rat Hepatocytes ◽

Butyl Hydroperoxide ◽

Primary Rat Hepatocytes ◽

Tert Butyl ◽

Tert Butyl Hydroperoxide ◽

Rubus Chingii

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Regucalcin counteracts tert-butyl hydroperoxide and cadmium-induced oxidative stress in rat testis

Journal of Applied Toxicology ◽

10.1002/jat.3333 ◽

2016 ◽

Vol 37 (2) ◽

pp. 159-166 ◽

Cited By ~ 12

Author(s):

Sara Correia ◽

Cátia V. Vaz ◽

Ana M. S. Silva ◽

José E. Cavaco ◽

Sílvia Socorro

Keyword(s):

Oxidative Stress ◽

Butyl Hydroperoxide ◽

Rat Testis ◽

Tert Butyl ◽

Tert Butyl Hydroperoxide

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Effects of Epigallocatechin Gallate on Tert-Butyl Hydroperoxide-Induced Mitochondrial Dysfunction in Rat Liver Mitochondria and Hepatocytes

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/7573131 ◽

2016 ◽

Vol 2016 ◽

pp. 1-8 ◽

Cited By ~ 3

Author(s):

Vojtech Mezera ◽

Rene Endlicher ◽

Otto Kucera ◽

Ondrej Sobotka ◽

Zdenek Drahota ◽

...

Keyword(s):

Mitochondrial Dysfunction ◽

Rat Liver ◽

Epigallocatechin Gallate ◽

Rat Hepatocytes ◽

Liver Mitochondria ◽

Rat Liver Mitochondria ◽

Retention Capacity ◽

Butyl Hydroperoxide ◽

Tert Butyl ◽

Tert Butyl Hydroperoxide

Epigallocatechin gallate (EGCG) is a green tea antioxidant with adverse effects on rat liver mitochondria and hepatocytes at high doses. Here, we assessed whether low doses of EGCG would protect these systems from damage induced by tert-butyl hydroperoxide (tBHP). Rat liver mitochondria or permeabilized rat hepatocytes were pretreated with EGCG and then exposed to tBHP. Oxygen consumption, mitochondrial membrane potential (MMP), and mitochondrial retention capacity for calcium were measured. First, 50 μM EGCG or 0.25 mM tBHP alone increased State 4 Complex I-driven respiration, thus demonstrating uncoupling effects; tBHP also inhibited State 3 ADP-stimulated respiration. Then, the coexposure to 0.25 mM tBHP and 50 μM EGCG induced a trend of further decline in the respiratory control ratio beyond that observed upon tBHP exposure alone. EGCG had no effect on MMP and no effect, in concentrations up to 50 μM, on mitochondrial calcium retention capacity. tBHP led to a decline in both MMP and mitochondrial retention capacity for calcium; these effects were not changed by pretreatment with EGCG. In addition, EGCG dose-dependently enhanced hydrogen peroxide formation in a cell- and mitochondria-free medium.Conclusion. Moderate nontoxic doses of EGCG were not able to protect rat liver mitochondria and hepatocytes from tBHP-induced mitochondrial dysfunction.

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