Catechol inhibits FADH2-linked respiration in rat liver mitochondrial fraction

Barreto, George E.; Santos, Gleide Souza dos; Egito, Eryvaldo Sócrates Tabosa do; El-Bachá, Ramon dos Santos

doi:10.1590/s0102-86502005000700008

Cited by 10 publications

(4 citation statements)

References 22 publications

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“…Studies conducted by Barreto et al [2005] demonstrated that catechol inhibits liver mitochondrial state 2 FADH 2 -linked respiration. These data suggest the inhibition of mitochondrial respiration by catechol as a potential mechanism of its cytotoxicity.…”

Section: Catechol and Dna Damage: An Oxidative Pathwaymentioning

confidence: 99%

The role of catechols and free radicals in benzene toxicity: An oxidative DNA damage pathway

Barreto

Madureira

Capani

et al. 2009

Environ and Mol Mutagen

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Benzene is a widespread volatile compound and an environmental contaminant. Since it causes important toxic effects in workers exposed to low levels, long-term exposure to this compound has been extensively studied. Leukemia, blood disorders, bone marrow depression, and some types of cancer are directly related to benzene-initiated toxicity. Bioactivation of benzene can lead to the formation of hazardous metabolites such as phenol, hydroquinone, and catechol. Catechol forms semiquinones and reactive quinones that are presumed to play an important role in the generation of reactive oxygen species (ROS). ROS formation can directly induce single and double strand breaks in the DNA, oxidized nucleotides, and hyper-recombination, and consequently produces deleterious genetic changes. In this review, we have addressed the cytotoxic effects of benzene and its main metabolite, catechol, focusing on the oxidative pathway and further DNA damage.

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Section: Catechol and Dna Damage: An Oxidative Pathwaymentioning

confidence: 99%

The role of catechols and free radicals in benzene toxicity: An oxidative DNA damage pathway

Barreto

Madureira

Capani

et al. 2009

Environ and Mol Mutagen

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“…The results also showed for the first time that 3MC significantly inhibited state 2 FADH 2 -linked respiration in rat brain nonsynaptic mitochondria. In a previous work, 1,2-dihydroxybenzene (catechol) also inhibited state 2 FADH 2 -linked respiration of rat liver mitochondria (Barreto et al, 2005). These data suggest that catechols may interfere with the respiratory chain.…”

Section: Discussionmentioning

confidence: 54%

Investigation of toxic factors affecting cells of rat brains exposed to 3-methylcatechol

Barreto

Oliveira

Villar

et al. 2007

Braz. arch. biol. technol.

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“…9 Although the aim of this work was not to study the effects of catechol on mitochondrial respiration in GL-15 cells, a previous work showed that catechol inhibited state 2 FADH 2 -linked respiration of rat liver mitochondria. 25 Furthermore, 3-methylcatechol also inhibited state 2 FADH 2 -linked respiration in rat brain nonsynaptic mitochondria. 26 Cells can die by two major mechanisms: necrosis or apoptosis.…”

Section: Discussionmentioning

confidence: 94%

Catechol cytotoxicity in vitro: Induction of glioblastoma cell death by apoptosis

et al. 2010

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The exposure to benzene is a public health problem. Although the most well-known effect of benzene is hematopoietic toxicity, there is little information about the benzene and its metabolites effects on the central nervous system (CNS). This study examined the toxic effects of 1,2-dihydroxybenzene (catechol), a benzene metabolite, to human glioblastoma GL-15 cells. GL-15 cell cultures were used as a model to provide more information about the toxic effects of aromatic compounds to the CNS. Catechol induced time- and concentration-dependent cytotoxic effects. Morphological changes, such as the retraction of the cytoplasm and chromatin clumping, were seen in cells exposed to 200 μM catechol for 48 hours. In cells exposed to 600 μM catechol for 48 hours, 78.0% of them presented condensed nuclei, and the Comet assay showed DNA damage. The percentage of cells labeled with annexin V (apoptotic cells) was greater in the group exposed to catechol (20.7%) than in control cells (0.4%). Exposure to catechol at concentrations greater than 100 μM enhanced Bax levels, and a decrease in Bcl-2 level was observed after the exposure to 600 μM catechol for 48 hours. Furthermore, catechol depleted reduced glutathione. Hence, catechol induced cell death mainly by apoptosis.

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Catechol inhibits FADH2-linked respiration in rat liver mitochondrial fraction

Abstract: Catechol produced an inhibition of basal respiration associated to FADH2 in isolated liver mitochondria that could lead to cytotoxicity, ROS generation and cell death.

Cited by 10 publications

References 22 publications

The role of catechols and free radicals in benzene toxicity: An oxidative DNA damage pathway

The role of catechols and free radicals in benzene toxicity: An oxidative DNA damage pathway

Investigation of toxic factors affecting cells of rat brains exposed to 3-methylcatechol

Catechol cytotoxicity in vitro: Induction of glioblastoma cell death by apoptosis

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