Benzyl Viologen-Mediated Counteraction of Diquat and Paraquat Phytotoxicities

Lewinsohn, Efraim; Gressel, Jonathan

doi:10.1104/pp.76.1.125

Cited by 25 publications

(10 citation statements)

References 19 publications

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“…These findings are consistent with the fact that cytochrome P450 reductase contains both FAD and FMN [28]. Of interest was our observation that diquat was more active than paraquat in generating hydrogen peroxide and hydroxyl radicals during redox cycling, a finding likely due to the more positive redox potential of diquat (-350 mV) when compared to paraquat (-446 mV) [6, 35]. For hydrogen peroxide and hydroxyl radical production, the apparent K M 's for diquat and paraquat redox cycling were lower with the recombinant enzyme, relative to the microsomes.…”

Section: Discussionsupporting

confidence: 85%

Redox cycling and increased oxygen utilization contribute to diquat-induced oxidative stress and cytotoxicity in Chinese hamster ovary cells overexpressing NADPH-cytochrome P450 reductase

Fussell

Udasin

Gray

et al. 2011

Free Radical Biology and Medicine

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Diquat and paraquat are non-specific defoliants that induce toxicity in many organs including the lung, liver, kidney and brain. This toxicity is thought to be due to the generation of reactive oxygen species (ROS). An important pathway leading to ROS production by these compounds is redox cycling. In the present studies, diquat and paraquat redox cycling was characterized using human recombinant NADPH-cytochrome P450 reductase, rat liver microsomes, and Chinese Hamster Ovary (CHO) cells constructed to overexpress cytochrome P450 reductase (CHO-OR) and wild type control cells (CHO-WT). In redox cycling assays with recombinant cytochrome P450 reductase and microsomes, diquat was 10-40 times more effective in generating ROS when compared to paraquat (KM = 1.0 and 44.2 μM, respectively for H2O2 generation by diquat and paraquat using recombinant enzyme, and 15.1 and 178.5 μM, respectively for microsomes). In contrast, at saturating concentrations, these compounds showed similar redox cycling activity (Vmax ≈ 6.0 nmoles H2O2/min/mg protein) for recombinant enzyme and microsomes. Diquat and paraquat also redox cycle in CHO cells. Significantly more activity was evident in CHO-OR cells than CHO-WT cells. Diquat redox cycling in CHO cells was associated with marked increases in protein carbonyl formation, a marker of protein oxidation, as well as cellular oxygen consumption, measured using oxygen microsensors; greater activity was detected in CHO-OR cells than CHO-WT cells. These data demonstrate that ROS formation during diquat redox cycling can generate oxidative stress. Enhanced oxygen utilization during redox cycling may reduce intracellular oxygen available for metabolic reactions and contribute to toxicity.

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Section: Discussionsupporting

confidence: 85%

Redox cycling and increased oxygen utilization contribute to diquat-induced oxidative stress and cytotoxicity in Chinese hamster ovary cells overexpressing NADPH-cytochrome P450 reductase

Fussell

Udasin

Gray

et al. 2011

Free Radical Biology and Medicine

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“…Superoxide dismutase in poplar leaves increases after exposure to sulfur dioxide and these leaves become more tolerant to sulfhur dioxide exposures (30). Paraquat, benzyl viologen, methyl viologen (agents which cause increases in the superoxide radical in cells) cause increases of superoxide dismutase (12,19,24). In our study, superoxide dismutase activity increased with fumigated trees having one and a half more enzyme activity than control trees after the 4 h fumigation (9.1 x 103 versus 14.1 x 103 units mg-' Chl, control and fumigated, respectively).…”

Section: Discussionmentioning

confidence: 99%

Response of Photosynthesis and Cellular Antioxidants to Ozone in Populus Leaves

Gupta¹,

Alscher²,

McCune³

1991

Plant Physiol.

123

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Atmospheric ozone causes formation of various highly reactive intermediates (e.g. peroxyl and superoxide radicals, H202, etc.) in plant tissues. A plant's productivity in environments with ozone may be related to its ability to scavenge the free radicals formed. The effects of ozone on photosynthesis and some free radical scavengers were measured in the fifth emergent leaf of poplars. Clonal poplars (Populus deltoides x Populus cv caudina) were fumigated with 180 parts per billion ozone for 3 hours. Photosynthesis was measured before, during, and after fumigation. During the first 90 minutes of ozone exposure, photosynthetic rates were unaffected but glutathione levels and superoxide dismutase activity increased. After 90 minutes of ozone exposure, photosynthetic rates began to decline while glutathione and superoxide dismutase continued to increase. Total glutathione (reduced plus oxidized) increased in fumigated leaves throughout the exposure period. The ratio of GSH/GSSG also decreased from 12.8 to 1.2 in ozone exposed trees. Superoxide dismutase levels increased twofold in fumigated plants. After 4 hours of ozone exposure, the photosynthetic rate was approximately half that of controls while glutathione levels and superoxide dismutase activity remained above that of the controls. The elevated antioxidant levels were maintained 21 hours after ozone exposure while photosynthetic rates recovered to about 75% of that of controls. Electron transport and NADPH levels remained unaffected by the treatment. Hence, elevated antioxidant metabolism may protect the photosynthetic apparatus during exposure to ozone.All organisms that have evolved in aerobic environments have a variety of enzymatic and nonenzymatic mechanisms to prevent oxidation of cellular components. It is quite probable that existing mechanisms for detoxifying oxyradicals are invoked in response to ozone since it causes the formation of some highly reactive oxyradicals in aqueous solutions, a major product being the superoxide anion (I1). The superoxide anion can be metabolized by several isozymes of superoxide dismutase found in plants (14). The hydrogen peroxide formed by this reaction is toxic. It can inactivate -SH containing enzymes (5, 13) or react with superoxide to form the hydroxyl radical, which can attack many macromolecular

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“…powerful oxidative metabolism of DQ and consequent enormous O 2 deprivation. Compared to paraquat (PQ) (widely used herbicide, bipyridylium analogue of DQ), DQ is a more powerful oxidant based on its redox potentials (E o '=-349 mV for DQ and E o '=-446 mV for PQ) and its intense oxidative metabolism probably underlies its harmful effects (Lewinson et al, 1984). Explicitly, DQ •+ reacts with O 2 , forming O 2…”

Section: Glutathione Peroxidase (Gpx)mentioning

confidence: 99%

Glutathione cycle in diquat neurotoxicity: Assessed by intrastriatal pre-treatment with glutathione reductase

Djurdjević¹,

Djukić²,

Ninković³

et al. 2013

ACTA VET-BEOGRAD

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Diquat (DQ) neurotoxicity mechanisms are unknown, although, it's systemic toxicity is mediated by free radical reactions. The role of glutathione cycle was assessed by glutathione reductase (GR) applied in the pre-treatment of DQ poisoning. Wistar rats were used and tested compounds were administered intrastriatally (i.s.) in one single dose. Total glutathione (tGSH), glutathione disulfide (GSSG) and glutathione peroxidase (GPx) were measured in the vulnerable brain regions (VBRs) (striatum, hippocampus and cortex), at 30 minutes, 24 hours and 7 days post treatment. Results from the intact and the sham operated groups were not statistically different. Rapid spatial spreading of oxidative stress was confirmed in the examined VBRs. Mortality (30-40%, within 24hrs) and signs of lethargy were observed in the DQ group. Activity of GPx activity was elevated and GSSG/GSH was higher in the examined VBRs during the experiment, compared to the controls. The i.s. pre-treatment with GR achieved neuroprotective role against DQ induced neurotoxicity, based on animal survival, absence of lethargy and decreased GPx activity and GSSG/GSH in the examined VBRs during the experiment, compared to the DQ group. Our results confirmed that oxidation of GSH was the reason for the reduced antioxidative defense against DQ neurotoxicity. [Projekat Ministarstva nauke Republike Srbije, br. III41018

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Benzyl Viologen-Mediated Counteraction of Diquat and Paraquat Phytotoxicities

Cited by 25 publications

References 19 publications

Redox cycling and increased oxygen utilization contribute to diquat-induced oxidative stress and cytotoxicity in Chinese hamster ovary cells overexpressing NADPH-cytochrome P450 reductase

Redox cycling and increased oxygen utilization contribute to diquat-induced oxidative stress and cytotoxicity in Chinese hamster ovary cells overexpressing NADPH-cytochrome P450 reductase

Response of Photosynthesis and Cellular Antioxidants to Ozone in Populus Leaves

Glutathione cycle in diquat neurotoxicity: Assessed by intrastriatal pre-treatment with glutathione reductase

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