Paraquat Treatment Research Articles

Reproductive activation in honeybee (Apis mellifera) workers protects against abiotic and biotic stress.

Social insect reproductives exhibit exceptional longevity instead of the classic trade-off between somatic maintenance and reproduction. Even normally sterile workers experience a significant increase in life expectancy when they assume a reproductive role. The mechanisms that enable the positive relation between the antagonistic demands of reproduction and somatic maintenance are unclear. To isolate the effect of reproductive activation, honeybee workers were induced to activate their ovaries. These reproductively activated workers were compared to controls for survival and gene expression patterns after exposure to Israeli Acute Paralysis Virus or the oxidative stressor paraquat. Reproductive activation increased survival, indicating better immunity and oxidative stress resistance. After qPCR analysis confirmed our experimental treatments at the physiological level, whole transcriptome analysis revealed that paraquat treatment significantly changed the expression of 1277 genes in the control workers but only two genes in reproductively activated workers, indicating that reproductive activation preemptively protects against oxidative stress. Significant overlap between genes that were upregulated by reproductive activation and in response to paraquat included prominent members of signalling pathways and anti-oxidants known to affect ageing. Thus, while our results confirm a central role of vitellogenin, they also point to other mechanisms to explain the molecular basis of the lack of a cost of reproduction and the exceptional longevity of social insect reproductives. Thus, socially induced reproductive activation preemptively protects honeybee workers against stressors, explaining their longevity. This article is part of the theme issue 'Ageing and sociality: why, when and how does sociality change ageing patterns?'

Progress in the study of pulmonary fibrosis signaling pathways caused by paraquat poisoning

Paraquat is a quaternary ammonium herbicide, which can be distributed in lung, liver, kidney, heart, brain and other organs through blood circulation, leading to multiple organ failure, especially lung injury. Due to the lack of effective treatment methods and specific antidotes, the prognosis of most patients with paraquat poisoning is very poor. The treatment of paraquat poisoning was a big problem for emergency doctors. Previous studies have found that pulmonary fibrosis caused by paraquat poisoning is closely related to a variety of pathological processes, such as oxidative stress, inflammatory reaction, mitochondrial damage, imbalance of extracellular matrixproduction (ECM) and degradation, which involve the activation or inhibition of various signaling pathways. In recent years, many researchers focused on clarifying the mechanism of paraquat induced pulmonary fibrosis, and some signaling pathways related to paraquat poisoning leading to pulmonary fibrosis have been found. A large number of studies have found that adenosine monophosphate activated protein kinase (AMPK) related signaling pathway, transforming growth factor-β/Smad (TGF-β/Smad) signaling pathway, mitogen-activated protein kinase (MAPK) related signaling pathway, Ras homolog gene/Rho associated kinases (Ras/ROCK) and Wnt/β-catenin signal pathways are closely related to paraquat induced pulmonary fibrosis. In this paper, we reviewed signaling pathways related to paraquat induced pulmonary fibrosis, in order to provide more ideas for the clinical treatment of paraquat induced pulmonary fibrosis.

20-hydroxyecdysone regulates expression of methioninesulfoxide reductases through transcription factor FOXO in the red flour beetle, Tribolium castaneum

The oxidation of methionine (Met) by reactive oxygen species (ROS) causes detrimental effects on the protein functions. Methionine sulfoxide reductase (Msr) is the secondary antioxidant enzyme involved in protein repair, and is divided into two distinct classes, MsrA and MsrB, although the mechanisms underlying the transcriptional regulation of Msrs remain largely unknown. In this study, the full-length cDNAs encoding MsrA and three alternatively spliced isoforms of MsrB were isolated from the red flour beetle, Tribolium castaneum. Exposure of female adults to oxidative, heat and cold stresses induced expressions of both MsrA and MsrB. RNAi-mediated knockdown of MsrA and MsrB resulted in increased sensitivity of T. castaneum to paraquat-induced oxidative stress. Treatment with 20-hydroxyecdysone (20E) increased expression levels of both MsrA and MsrB. Knockdown of transcription factor forkhead box O (FOXO) decreased both MsrA and MsrB mRNA levels and abolished the induction of MsrA and MsrB by paraquat. Luciferase reporter assays revealed that FOXO directly activates the promoters of both MsrA and MsrB. Moreover, paraquat treatment induced expression of two ecdysone biosynthesis genes, Shade and Phantom, 20E upregulated exoression of FOXO, promoted FOXO nuclear translocation，and knockdown of FOXO abolished induction of MsrA and MsrB expression by 20E, suggesting that regulation of MsrA and MsrB by 20E was mediated by FOXO. Overall, these results provide important insights into the transcriptional regulation of insect Msrs.

Paraquat herbicide diminishes chemoreflex sensitivity, induces cardiac autonomic imbalance and impair cardiac function in rats.

Paraquat (PQT) herbicide is widely used in agricultural practices despite being highly toxic to humans. It has been proposed that PQT exposure may promote cardiorespiratory impairment. However, the physiological mechanisms involved in cardiorespiratory dysfunction following PQT exposure are poorly known. We aimed to determine the effects of PQT on ventilatory chemoreflex control, cardiac autonomic control, and cardiac function in rats. Male Sprague-Dawley rats received two injections/week of PQT (5 mg·kg-1 ip) for 4 wk. Cardiac function was assessed through echocardiography and pressure-volume loops. Ventilatory function was evaluated using whole body plethysmography. Autonomic control was indirectly evaluated by heart rate variability (HRV). Cardiac electrophysiology (EKG) and exercise capacity were also measured. Four weeks of PQT administration markedly enlarged the heart as evidenced by increases in ventricular volumes and induced cardiac diastolic dysfunction. Indeed, end-diastolic pressure was significantly higher in PQT rats compared with control (2.42 ± 0.90 vs. 4.01 ± 0.92 mmHg, PQT vs. control, P < 0.05). In addition, PQT significantly reduced both the hypercapnic and hypoxic ventilatory chemoreflex response and induced irregular breathing. Also, PQT induced autonomic imbalance and reductions in the amplitude of EKG waves. Finally, PQT administration impaired exercise capacity in rats as evidenced by a ∼2-fold decrease in times-to-fatigue compared with control rats. Our results showed that 4 wk of PQT treatment induces cardiorespiratory dysfunction in rats and suggests that repetitive exposure to PQT may induce harmful mid/long-term cardiovascular, respiratory, and cardiac consequences.NEW & NOREWORTHY Paraquat herbicide is still employed in agricultural practices in several countries. Here, we showed for the first time that 1 mo paraquat administration results in cardiac adverse remodeling, blunts ventilatory chemoreflex drive, and promotes irregular breathing at rest in previously healthy rats. In addition, paraquat exposure induced cardiac autonomic imbalance and cardiac electrophysiology alterations. Lastly, cardiac diastolic dysfunction was overt in rats following 1 mo of paraquat treatment.

Further evaluation of herbicides in yam (Dioscorea sp.)

Two trials were carried out during 1986-87 at the Corozal substation to evaluate six herbicides for weed control in yam. In the first test, herbicides evaluated were ametryn, fluazifop-P, oxyfluorfen and paraquat. Ametryn at 4.48 kg ai/ha, in sequential application with fluazifop-P at 0.56 kg ai/ha, was highly effective against broadleaf weeds. Oxyfluorfen alone and oxyfluorfen + paraquat were also highly effective, but both treatments caused slight to moderate crop injury. In the second trial, ametryn, fluazifop-P, paraquat, cinmethylin and metolachor were evaluated. Ametryn at 4.48 kg ai/ha in sequential application with fluazifop at 0.84 kg ai/ha again proved to be highly effective. Cinmethylin alone was poor against broadleaf weeds. Its sequential application with paraquat slightly improved weed control. Metolachor at 3.54 and 7.08 L/ha+ paraquat also provided good weed control. Its sequential application with paraquat slightly improved weed control. Metolachor at 3.54 and 7.08 L/ha + paraquat also provided good weed control. In the first planting there were no significant differences in tuber yield between the weeded check and other herbicide treatments except for the fluazifop-P alone treatments. In the second planting, with the exception of the cinmethylin alone treatments and one of the cinmethylin + paraquat treatments, there were no significant yield differences between the weeded check and the herbicide treatments.

Capacitive Deionization for the Removal of Paraquat Herbicide from Aqueous Solution

In comparison to other conventional methods like adsorption and reverse osmosis (RO), capacitive deionization (CDI) has only been investigated extensively for the removal of inorganic pollutants from water, demonstrating limited practicality. Herein, the study investigated the use of CDI for the removal of paraquat (PQ) herbicide from water by using commercial activated carbon (AC) electrodes. The CDI performance was examined as a function of the initial PQ concentration, applied voltage, flowrate, treatment time, and cycle stability testing in the batch mode approach. The applied voltage had a beneficial effect on the removal efficiency, whereas the removal efficiency of PQ declined as the initial PQ concentration increased. However, the electrosorption capacity gradually increased with the increase of initial feed solutions’ concentration. The maximum removal efficiency and electrosorption capacity achieved at 5 mg/L and 20 mg/L PQ initial concentrations, an applied voltage of 1.2 V, and 5 mL/min flowrate were 100% and 0.33 mg/g and 52.5% and 0.7 mg/g, respectively. Washing the electrodes with distilled water achieved sequential desorption of PQ, and the process produces a waste stream that can be disposed of or treated further. Therefore, the CDI method is considered a promising and efficient method for removing organic pollutants from water including pesticides.

Effect of paraquat treatment on reactive oxygen species and antioxidant enzyme activity in Caenorhabditis elegans

Effect of paraquat treatment on reactive oxygen species and antioxidant enzyme activity in Caenorhabditis elegans

Suppression of tau-induced phenotypes by vitamin E demonstrates the dissociation of oxidative stress and phosphorylation in mechanisms of tau toxicity.

Various lines of evidence implicate oxidative stress in the pathogenic mechanism(s) underpinning tauopathies. Consequently, antioxidant therapies have been considered in clinical practice for the treatment of tauopathies such as Alzheimer's disease (AD), but with mixed results. We and others have previously reported increased protein oxidation upon expression of both human 0N3R (hTau0N3R ) and 0N4R (hTau0N4R ) tau in vivo. Building on these studies, we demonstrate here the suppression of hTau0N3R associated phenotypes in Drosophila melanogaster after treatment with vitamin C or vitamin E. Curiously the rescue of phenotype was seen without alteration in total tau level or alteration in phosphorylation at a number of disease-associated sites. Moreover, treatment with paraquat, a pro-oxidant drug, did not exacerbate the hTau0N3R phenotypes. This result following paraquat treatment is reminiscent of our previous findings with hTau0N4R which also causes greater oxidative stress when compared to hTau0N3R but has a milder phenotype. Collectively our data imply that the role of oxidative stress in tau-mediated toxicity is not straight forward and there may be isoform-specific effects as well as contribution of other factors. This may explain the ambiguous effects of anti-oxidant treatments on clinical outcome in dementia patients.

Paraquat Treatment Compromises the Clearance of β-Amyloid and Tau Proteins and Induces Primary Hippocampal Neuronal Cell Death through HSP70, P20S, and TFEB Disruption.

The herbicide paraquat (PQ) induces hippocampal neuronal cell loss and cognitive dysfunction after one and repeated treatment. All the mechanisms involved in these effects are not well understood. Single and repeated PQ treatment increased Aβ and tau protein levels, through HSP70 and TFEB downregulation and proteasome 20S inhibition, producing cell death in primary hippocampal neurons associated with cognitive decline. Our results reveal the mechanisms through which PQ could induce the accumulation of abnormal proteins and neurodegeneration that could originate the cognitive decline produced by it and could help managing its degenerative effects.

Identification of a new P450s gene (AccCYP4AV1) and its roles in abiotic stress resistance in the Apis cerana cerana Fabricius.

Cytochrome P450 monooxygenases (P450s) play significant roles in protecting organisms from abiotic stress damage. Here, we report the sequence and characterization of a P450s gene (AccCYP4AV1), isolated from Apis cerana cerana Fabricius. The open reading frame of AccCYP4AV1 is 1506 base pairs long and encodes a predicted protein of 501 amino acids and 57.84 kDa, with an isoelectric point of 8.67. Real-time quantitative polymerase chain reaction (RT-qPCR) analysis indicated that AccCYP4AV1 is more highly expressed in the midgut than in other tissues. In addition, the highest expression occurs in newly emerged adult workers, followed by the first instar of the larval stage. In addition, the expression of the AccCYP4AV1 was upregulated by low temperature (4 °C), ultraviolet radiation, hydrogen peroxide, paraquat, and dichlorvos treatments. In contrast, AccCYP4AV1 transcription was downregulated by other abiotic stress conditions: exposure to increased temperature (44 °C), deltamethrin, cadmium chloride, and mercury (II) chloride. Moreover, when AccCYP4AV1 was knocked-down by RNA interference, the results suggested that multiple antioxidant genes (AccsHSP22.6, AccSOD2, AccTpx1, and AccTpx4) were downregulated and antioxidant genes AccGSTO1 and AccTrx1 were upregulated. The activity levels of peroxidase and catalase were upregulated in the AccCYP4AV1-knocked-down samples, compared with those in the control groups. These findings suggest that the AccCYP4AV1 protein might be involved in the defense against abiotic stress damage.

The PARK2 Mutation Associated with Parkinson's Disease Enhances the Vulnerability of Peripheral Blood Lymphocytes to Paraquat.

Parkinson's disease (PD) is the second most common neurodegenerative disease in middle-aged and elderly people. However, the etiology and pathogenesis of PD are still unclear and there is a lack of reliable biomarkers for early molecular diagnosis. Parkin (encoded by PARK2) is a ubiquitin E3 ligase that participates in mitochondrial homeostasis, the ubiquitin-proteasome pathway, oxidative stress response, and cell death pathways, which are involved in the pathogenesis of PD. However, Parkin is also expressed in peripheral blood lymphocytes (PBLs). In this study, permanent lymphocyte lines were established from the peripheral blood of sporadic PD (sPD) patients, PARK2 mutation carriers, and healthy controls. Reactive oxygen species (ROS), function of the mitochondrial respiratory chain complex I, and apoptosis were analyzed in the PBLs. There was no significant difference in ROS, mitochondrial respiratory chain complex I, and apoptosis between the experimental groups and the control group without paraquat treatment. Compared with the control group of healthy subjects, we found an increase of ROS (control 100 ± 0, sPD 275.53 ± 79.11, and C441R 340 ± 99.67) and apoptosis, as well as a decline in the function of mitochondrial respiratory chain complex I in PBLs of PARK2 mutation carriers and sPD after the treatment of paraquat (control 0.65 ± 0.08, sPD 0.44 ± 0.08, and C441R 0.32 ± 0.08). Moreover, overexpression of the wild-type (WT) PARK2 in HeLa cells and immortalized PBLs could rescue mitochondrial function and partially inhibit apoptosis following paraquat treatment, while the C441R mutation could not. Thus, ROS levels, activity of mitochondrial respiratory chain complex I, and apoptosis of PBLs are potential diagnostic biomarkers of PD.

Inhibition of TBK1 by amlexanox attenuates paraquat-induced acute lung injury

The specific mechanism of paraquat (PQ)-induced acute lung injury (ALI) is unclear, though inflammation is a likely contributor. Amlexanox, a TANK binding kinase 1 (TBK1) inhibitor, is a strong anti-inflammatory drug. We investigated the role of TBK1 and the potential therapeutic effect of amlexanox in the pathogenesis of PQ-induced ALI. After 30 mg/kg PQ treatment for 72 h, mouse lung pathological injury occurred, and the protein concentration in alveolar lavage fluid was increased. Next, RAW264.7 mouse macrophages were treated with 100 μM PQ for 24 h, which decreased cell viability. PQ induced oxidative damage and increased IL-1β, IFNβ, NF-κBp65, IRF3, and pTBK1/TBK1 levels in mouse lungs and RAW264.7 cells. Inhibiting the activation of TBK1 with amlexanox (100 mg/kg in mice and 50 μM in RAW264.7 cells) attenuated mouse lung injury and decreased the protein concentration in alveolar lavage fluid. Further, amlexanox relieved the oxidative damage in mouse lungs and RAW264.7 cells, reduced the levels of inflammatory factors such as IL-1β and IFNβ, and inhibited the activation of NF-κBp65 and IRF3. These results suggest that TBK1 plays a key role in the pathogenesis of PQ-induced ALI. Further, amlexanox treatment alleviates PQ-induced ALI by inhibiting the TBK1-NF-κB/IRF3 signalling pathway. Our study provides evidence that TBK1 inhibition by amlexanox alleviates PQ-induced ALI and may be a new therapeutic strategy.

FoxF1 protects rats from paraquat-evoked lung injury following HDAC2 inhibition via the microRNA-342/KLF5/IκB/NF-κB p65 axis

PurposeForkhead box f1 (FoxF1), a transcription factor, was implicated in lung development. However, the molecular mechanism of FoxF1 in lung injury, specifically in injury caused by paraquat (PQ), one of the most frequently used herbicides, is unknown. Accordingly, we performed this study to investigate whether FoxF1 attenuates PQ-induced lung injury and to determine the possible mechanism. MethodsWe used PQ-treated Beas-2B cells to measure the expression of FoxF1. Later, ChIP-qPCR was applied to detect the levels of histone acetylation in cells, followed by the validation of the relationship between histone deacetylase-2 (HDAC2) and FoxF1. Subsequently, the correlation between FoxF1 and microRNA (miR)-342 and the downstream mechanism of miR-342 were evaluated by bioinformatics analysis. The apoptosis and the content of reactive oxygen species (ROS) in PQ-treated cells were detected to evaluate the roles of HDAC2, FoxF1 and miR-342 in vitro. Finally, a rat model was developed to evaluate the effects of HDAC2, miR-342 and Krüppel-like factor 5 (KLF5) on PQ-induced lung injury in vivo. ResultsPQ treatment significantly enhanced FoxF1 promoter deacetylation, thereby inhibiting FoxF1 expression. After inhibition of HDAC2 activity, apoptosis and oxidative stress induced by PQ were significantly reversed. Nevertheless, further inhibition of miR-342 or overexpression of KLF5 promoted apoptosis and oxidative stress induced by PQ, and IκB/NF-κB p65 signaling was significantly activated after PQ treatment. ConclusionPQ treatment inhibited miR-342 expression by promoting HDAC2-induced deacetylation of the FoxF1 promoter, thereby promoting KLF5 expression and the IκB/NF-κB p65 signaling activation, and finally exacerbating PQ-induced lung injury in rats.

Dysregulation of prostaglandine E2 and BDNF signaling mediated by estrogenic dysfunction induces primary hippocampal neuronal cell death after single and repeated paraquat treatment

Paraquat (PQ) produces hippocampal neuronal cell death and cognitive dysfunctions after unique and continued exposure, but the mechanisms are not understood. Primary hippocampal wildtype or βAPP-Tau silenced cells were co-treated with PQ with or without E2, N-acetylcysteine (NAC), NS-398 (cyclooxygenase-2 inhibitor), MF63 (PGES-1 inhibitor) and/or recombinant brain-derived neurotrophic factor (BDNF) during one- and fourteen-days to studied PQ effect on prostaglandin E2 (PGE2) and BDNF signaling and their involvement in hyperphosphorylated Tau (pTau) and amyloid-beta (Aβ) protein formation, and oxidative stress generation, that lead to neuronal cell loss through estrogenic disruption, as a possible mechanism of cognitive dysfunctions produced by PQ. Our results indicate that PQ overexpressed cyclooxygenase-2 that leads to an increase of PGE2 and alters the expression of EP1-3 receptor subtypes. PQ induced also a decrease of proBDNF and mature BDNF levels and altered P75NTR and tropomyosin receptor kinase B (TrkB) expression. PQ induced PGE2 and BDNF signaling dysfunction, mediated through estrogenic disruption, leading to Aβ and pTau proteins synthesis, oxidative stress generation and finally to cell death. Our research provides relevant information to explain PQ hippocampal neurotoxic effects, indicating a probable explanation of the cognitive dysfunction observed and suggests new therapeutic strategies to protect against PQ toxic effects.

The MUC5B Mucin Is Involved in Paraquat-Induced Lung Inflammation.

Objective Paraquat (PQ), a widely used toxic herbicide, induces lung inflammation through mechanisms that remain incompletely understood. In a previous study, we found that the plasma MUC5B mucin level was implicated in PQ poisoning in patients. Here, we hypothesize that MUC5B is a critical mediator in PQ-induced cell inflammation. Methods A mouse model of PQ-induced lung injury was used to examine the MUC5B expression level. A549 cells (alveolar epithelial cells line) were exposed to PQ in dose-dependent and time-dependent manners. Cell viability was detected by CCK-8 assays. The expression levels of MUC5B were examined by dot blot enzyme-linked immunosorbent assay (ELISA) and RT-qPCR. Western blotting was used to detect the levels of proteins in the MAPK and NF-κB pathways. Inflammatory factors in the cell culture medium were measured by ELISA. NF-κB and MAPK pathway inhibitors and MUC5B siRNA (siMUC5B) were used to determine the function of MUC5B. Finally, N-acetyl-cysteine (NAC) was added and its regulatory effect on the MAPK-NF-κB-MUC5B pathway was examined in PQ-induced cell inflammation. Results MUC5B was significantly upregulated accompanying the increases in TNF-α and IL-6 secretion following PQ treatment in mouse and also in A549 cells after treatment with 50 μM PQ at 24 hours. Furthermore, MAPK and NF-κB pathway inhibitors could dramatically decrease the expression of MUC5B and the secretion of TNF-α and IL-6. Importantly, siMUC5B could significantly attenuate the secretion of TNF-α and IL-6 induced by PQ. As expected, the addition of NAC efficiently suppresses the TNF-α and IL-6 secretion stimulated from PQ and also downregulated ERK, JNK, and p65 phosphorylation (ERK/JNK MAPK and NF-κB pathways) as well as MUC5B expression. Conclusion Our findings suggest that MUC5B participates in the process of PQ-induced cell inflammation and is downstream of the NF-κB and MAPK pathways. NAC can attenuate PQ-induced cell inflammation at least in part by suppressing the MAPK-NF-κB-MUC5B pathway. These results nominate MUC5B as a new biomarker and therapeutic target for PQ-induced lung inflammation.

Mitochondria-Associated Degradation Pathway (MAD) Function beyond the Outer Membrane

SUMMARYThe mitochondria-associated degradation pathway (MAD) mediates ubiquitination and degradation of mitochondrial outer membrane (MOM) proteins by the proteasome. We find that the MAD, but not other quality-control pathways including macroautophagy, mitophagy, or mitochondrial chaperones and proteases, is critical for yeast cellular fitness under conditions of paraquat (PQ)-induced oxidative stress in mitochondria. Specifically, inhibition of the MAD increases PQ-induced defects in growth and mitochondrial quality and decreases chronological lifespan. We use mass spectrometry analysis to identify possible MAD substrates as mitochondrial proteins that exhibit increased ubiquitination in response to PQ treatment and inhibition of the MAD. We identify candidate substrates in the mitochondrial matrix and inner membrane and confirm that two matrix proteins are MAD substrates. Our studies reveal a broader function for the MAD in mitochondrial protein surveillance beyond the MOM and a major role for the MAD in cellular and mitochondrial fitness in response to chronic, low-level oxidative stress in mitochondria.

SSADH Variants Increase Susceptibility of U87 Cells to Mitochondrial Pro-Oxidant Insult

Succinate semialdehyde dehydrogenase (SSADH) is a mitochondrial enzyme, encoded by ALDH5A1, mainly involved in γ-aminobutyric acid (GABA) catabolism and energy supply of neuronal cells, possibly contributing to antioxidant defense. This study aimed to further investigate the antioxidant role of SSADH, and to verify if common SNPs of ALDH5A1 may affect SSADH activity, stability, and mitochondrial function. In this study, we used U87 glioblastoma cells as they represent a glial cell line. These cells were transiently transfected with a cDNA construct simultaneously harboring three SNPs encoding for a triple mutant (TM) SSADH protein (p.G36R/p.H180Y/p.P182L) or with wild type (WT) cDNA. SSADH activity and protein level were measured. Cell viability, lipid peroxidation, mitochondrial morphology, membrane potential (ΔΨ), and protein markers of mitochondrial stress were evaluated upon Paraquat treatment, in TM and WT transfected cells. TM transfected cells show lower SSADH protein content and activity, fragmented mitochondria, higher levels of peroxidized lipids, and altered ΔΨ than WT transfected cells. Upon Paraquat treatment, TM cells show higher cell death, lipid peroxidation, 4-HNE protein adducts, and lower ΔΨ, than WT transfected cells. These results reinforce the hypothesis that SSADH contributes to cellular antioxidant defense; furthermore, common SNPs may produce unstable, less active SSADH, which could per se negatively affect mitochondrial function and, under oxidative stress conditions, fail to protect mitochondria.

Nitrogen fertilizer programs following rice exposure to a sub-lethal concentration of paraquat

AbstractOff-target paraquat movement to rice has become a major problem in recent years for rice producers in the midsouthern United States. Nitrogen (N) fertilizer is applied to rice in greater quantity and frequency than all other nutrients to optimize rice yield. Two separate field studies were conducted from 2015 to 2018 in Stoneville, MS, to assess whether starter N fertilizer can aid rice recovery from exposure to a sub-lethal concentration of paraquat and to evaluate rice response to different N fertilizer management strategies following exposure to a sub-lethal concentration of paraquat. In both studies, paraquat treatments consisted of paraquat at 0 and 84 g ai ha–1 applied to rice in the two- to three-leaf (EPOST) growth stage. In the starter fertilizer study, N fertilizer at 24 kg ha–1 as ammonium sulfate (AMS) was applied to rice at spiking- to one-leaf (VEPOST), two- to three-leaf (EPOST), or three- to four-leaf (MPOST) growth stages before and after paraquat treatment. In the N fertilizer timing study, N fertilizer at 168 kg N ha–1 was applied in a single four-leaf to one-tiller (LPOST) application or two-, three-, and two four-way split applications. Despite starter N fertilizer applications, paraquat injured rice ≥41%, reduced height 57%, reduced dry weight prior to flooding 77%, delayed maturity 10 d, reduced dry weight at maturity 33%, and reduced rough rice yield 35% in the starter fertilizer study. Similarly, in the N fertilizer timing study, paraquat injured rice ≥45%, reduced height 14%, delayed maturity 10 d, reduced dry weight at maturity 44%, and reduced rough rice yield 50% for all N fertilizer management strategies. Both studies indicate that severe complications in growth and development can occur from rice exposure to a sub-lethal concentration of paraquat. In both studies, manipulation of N fertilizer management did not facilitate rice recovery from early-season exposure to paraquat.

Increased basal antioxidant levels in RCAN1 – deficient mice lowers oxidative injury after acute paraquat insult

RCAN1 is an inhibitor of the phosphatase calcineurin, which is involved in the regulation of oxidative stress and apoptosis, among other important cell processes. Here we have used RCAN1 deficient mice (RCAN1-/-) to elucidate its role after an acute oxidative insult such as paraquat injection. We have observed that RCAN1-/- mice show less oxidative damage than wildtype (WT) mice after treatment. Under basal conditions, RCAN1-/- animals express more calcineurin, heme oxygenase-1, Nrf2, and catalase compared to WT mice (controls). This may explain the less severe effect of paraquat treatment on RCAN1-/- mice compared to WT. We showed that oxidative stress is involved in the early stages of apoptosis, thus we determined the apoptotic effector BAD and found that decreases in RCAN1-/- mice after treatment with paraquat compared with WT in similar experimental conditions. Our results suggest that RCAN1 may be involved in the balance between oxidant and antioxidant species production in vivo.

Efficacy of hemoperfusion combined with continuous veno-venous hemofiltration on the treatment of paraquat poisoning: a Meta-analysis

To evaluate the efficacy of hemoperfusion (HP) combined with continuous veno-venous hemofiltration (CVVH) on the treatment of acute paraquat (PQ) poisoning. Prospective randomized controlled trials and retrospective studies on the efficacy of HP combined CVVH in patients with oral PQ poisoning (poisoning time ≤ 24 hours) were found by searching from PubMed, Embase, Cochrane Library, Web of Science, SinoMed, CNKI and Wanfang databases before November 1st, 2019. The experimental group was treated with HP+CVVH, and the control group was treated with HP. Data included the general information of the literature, mortality, survival time, the incidence of respiratory failure and circulatory failure. The bias risk and the data were analyzed using the RevMan 5.3 software. A total of 1 041 literatures were retrieved, and 7 literatures were finally enrolled, including 1 199 patients, with 735 patients in the control group and 464 patients in experimental group. Meta-analysis showed that compared with HP alone, HP+CVVH could significantly reduce the short-term mortality [4-day mortality: hazard ratio (HR) = 0.52, 95% confidence interval (95%CI) was 0.38-0.71, P < 0.000 1], but no significant improvement in long-term mortality was found (28-day or 30-day mortality: HR = 0.68, 95%CI was 0.39-1.21, P = 0.19; 90-day mortality: HR = 1.13, 95%CI was 0.61-2.10, P = 0.07; total mortality: HR = 0.96, 95%CI was 0.72-1.29, P = 0.78). The survival time of patients treated with HP+CVVH was significantly longer than that of HP patients [mean difference (MD) = 2.02, 95%CI was 0.81-3.22, P = 0.001], but the heterogeneity between studies was large. According to the type of literature, a subgroup analysis showed that the survival time of patients treated with HP+CVVH in prospective randomized controlled trials and retrospective studies were significantly longer than that of HP patients (prospective studies: MD = 1.53, 95%CI was 0.94-2.12, P < 0.000 01; retrospective studies: MD = 2.40, 95%CI was 0.08-4.73, P = 0.04). Compared with HP group, HP+CVVH could significantly reduce the incidence of circulatory failure [relative risk (RR) = 0.40, 95%CI was 0.30-0.52, P < 0.00 01], but the incidence of respiratory failure significantly increased (RR = 2.75, 95%CI was 2.18-3.48, P < 0.000 01). HP combined with CVVH can reduce the short-term mortality and the incidence of circulatory failure, prolong the survival time, and save time for further rescue, but it can't improve the long-term prognosis of patients.