ubiquinone and 4-nitrobenzoic-acid

ubiquinone has been researched along with 4-nitrobenzoic-acid* in 2 studies

Other Studies

2 other study(ies) available for ubiquinone and 4-nitrobenzoic-acid

Article	Year
Effects of inhibiting CoQ10 biosynthesis with 4-nitrobenzoate in human fibroblasts. PloS one, 2012, Volume: 7, Issue:2 Coenzyme Q(10) (CoQ(10)) is a potent lipophilic antioxidant in cell membranes and a carrier of electrons in the mitochondrial respiratory chain. We previously characterized the effects of varying severities of CoQ(10) deficiency on ROS production and mitochondrial bioenergetics in cells harboring genetic defects of CoQ(10) biosynthesis. We observed a unimodal distribution of ROS production with CoQ(10) deficiency: cells with <20% of CoQ(10) and 50-70% of CoQ(10) did not generate excess ROS while cells with 30-45% of CoQ(10) showed increased ROS production and lipid peroxidation. Because our previous studies were limited to a small number of mutant cell lines with heterogeneous molecular defects, here, we treated 5 control and 2 mildly CoQ(10) deficient fibroblasts with varying doses of 4-nitrobenzoate (4-NB), an analog of 4-hydroxybenzoate (4-HB) and inhibitor of 4-para-hydroxybenzoate:polyprenyl transferase (COQ2) to induce a range of CoQ(10) deficiencies. Our results support the concept that the degree of CoQ(10) deficiency in cells dictates the extent of ATP synthesis defects and ROS production and that 40-50% residual CoQ(10) produces maximal oxidative stress and cell death. Topics: Adenosine Triphosphate; Cell Death; Dose-Response Relationship, Drug; Fibroblasts; Humans; Nitrobenzoates; Oxidative Stress; Reactive Oxygen Species; Ubiquinone	2012
4-Nitrobenzoate inhibits coenzyme Q biosynthesis in mammalian cell cultures. Nature chemical biology, 2010, Volume: 6, Issue:7 Coenzyme Q (Q) is an electron transporter in the respiratory chain and a lipid-soluble antioxidant that decreases in humans with age. Here we show that 4-nitrobenzoate inhibited 4-hydroxybenzoate:polyprenyl transferase (Coq2) in a competitive manner and dose-dependently decreased Q in mammalian cells without accumulation of Q intermediates. As 4-nitrobenzoate neither interfered with mitochondrial respiration nor induced oxidative stress, it should prove a valuable tool for studies on both Q deficiency and Q supplementation. Topics: 3T3 Cells; Animals; Dose-Response Relationship, Drug; Gene Expression Regulation; Mice; Nitrobenzoates; Ubiquinone	2010

Article

Year

Effects of inhibiting CoQ10 biosynthesis with 4-nitrobenzoate in human fibroblasts.

PloS one, 2012, Volume: 7, Issue:2

Coenzyme Q(10) (CoQ(10)) is a potent lipophilic antioxidant in cell membranes and a carrier of electrons in the mitochondrial respiratory chain. We previously characterized the effects of varying severities of CoQ(10) deficiency on ROS production and mitochondrial bioenergetics in cells harboring genetic defects of CoQ(10) biosynthesis. We observed a unimodal distribution of ROS production with CoQ(10) deficiency: cells with <20% of CoQ(10) and 50-70% of CoQ(10) did not generate excess ROS while cells with 30-45% of CoQ(10) showed increased ROS production and lipid peroxidation. Because our previous studies were limited to a small number of mutant cell lines with heterogeneous molecular defects, here, we treated 5 control and 2 mildly CoQ(10) deficient fibroblasts with varying doses of 4-nitrobenzoate (4-NB), an analog of 4-hydroxybenzoate (4-HB) and inhibitor of 4-para-hydroxybenzoate:polyprenyl transferase (COQ2) to induce a range of CoQ(10) deficiencies. Our results support the concept that the degree of CoQ(10) deficiency in cells dictates the extent of ATP synthesis defects and ROS production and that 40-50% residual CoQ(10) produces maximal oxidative stress and cell death.

Topics: Adenosine Triphosphate; Cell Death; Dose-Response Relationship, Drug; Fibroblasts; Humans; Nitrobenzoates; Oxidative Stress; Reactive Oxygen Species; Ubiquinone

2012

4-Nitrobenzoate inhibits coenzyme Q biosynthesis in mammalian cell cultures.

Nature chemical biology, 2010, Volume: 6, Issue:7

Coenzyme Q (Q) is an electron transporter in the respiratory chain and a lipid-soluble antioxidant that decreases in humans with age. Here we show that 4-nitrobenzoate inhibited 4-hydroxybenzoate:polyprenyl transferase (Coq2) in a competitive manner and dose-dependently decreased Q in mammalian cells without accumulation of Q intermediates. As 4-nitrobenzoate neither interfered with mitochondrial respiration nor induced oxidative stress, it should prove a valuable tool for studies on both Q deficiency and Q supplementation.

Topics: 3T3 Cells; Animals; Dose-Response Relationship, Drug; Gene Expression Regulation; Mice; Nitrobenzoates; Ubiquinone

2010