Paraquat toxicity is reduced by polyamines in rice leaves

The protective effect of polyamines against paraquat (PQ) toxicity of rice (Oryza sativa) leaves was investigated. PQ treatment resulted in a higher putrescine (PUT) and lower spermidine (SPD) and spermine (SPM) levels in rice leaves. Pretreatment with SPD and SPM, which resulted in a 10- and 20-fold increase in endogenous level of SPD and SPM, respectively, reduced PQ toxicity (30%). Limited reduction of PQ toxicity by exogenous SPD and SPM is most likely due to the fact that they are not readily transported in rice leaf cells and localized to those areas along the cut edges of detached rice leaves [4]. PUT pretreatment did not increase endogenous SPD and SPM levels and had no effect on reducing PQ toxicity. It was found that 1,10-phenanthroline, an iron chelator, treatment reduced the toxicity of PQ (35%) and increased the levels of SPD (27%). The results indicate that reduction of PQ toxicity by SPD and SPM is due to increased activities of catalase (18%) and peroxidase (40%).     

Paraquat toxicity is reduced by metal chelators in rice leaves

The possible mediatory role of transition metals in paraquat (PQ) toxicity in rice leaves was investigated. Metal chelators (2,2'-bipyridine, 8-hydroxylquinoline and 1,10-phenanthroline) reduced PQ toxicity in rice leaves. The reduction of PQ toxicity by 1,10-phenanthroline (PA) is closely associated with the decrease in lipid peroxidation and increase in activities of enzymes detoxifying active oxygen species. Our results support the notion that iron or copper plays a major role in PQ toxicity in detached rice leaves. Reduction of PQ toxicity by PA in detached rice leaves is most likely mediated through chelation of iron or copper and an increase in superoxide dismutase and glutathione reductase activities.     

Paraquat toxicity and pyridine nucleotide coenzyme synthesis: a data correction

The decrease in pyridine nucleotide coenzymes which occurs during poisoning of Escherichia coli by hyperbaric oxygen or paraquat is not due to impairment of nicotinatemononucleotide pyrophosphorylase (carboxylating) [EC 2.4.2.19] as was previously proposed (Brown, O.R. et al. Biochem. Biophys. Res. Commun. 91:982-990; 1979). This was shown directly using extracts of E. coli, prepared after exposure to 1 mM paraquat or 4.2 atmospheres of oxygen. The enzyme also was not impaired in Neurospora crassa by 1 mM paraquat. A naturally-occurring, non-dialyzable inhibitor of the enzyme was found in E. coli extracts. The inhibitor caused the erroneous, low nicotinatemononucleotide pyrophosphorylase (carboxylating) activities previously reported in extracts of E. coli poisoned by paraquat.     

Paraquat toxicity in Pisum sativum: Effects on soluble and membrane-bound proteins

The effects of paraquat (PQ) on Pisum sativum L. proteins were investigated in vivo in a new experimental system utilizing 10-day-old plant cuts.A marked decrease in the specific activity of membrane-bound Ca²⁺-dependent ATPase was recorded, while that of Mg²⁺-dependent ATPase remained unchanged. Concurrently with a drop in the total plant protein, the specific activities of the three cytoplasmic enzymes, malate dehydrogenase, hydroxypyruvate reductase and triose-phosphate isomerase, were also found to decrease. The effect on various enzymes involved in cellular defense mechanisms was also studied: glutathione reductase and superoxide dismutase activities increased, while ascorbate peroxidase was not affected.
These findings shed light on the selectivity of PQ-induced injurious processes, focusing on protein homeostasis mechanisms in the membrane and cytoplasmic compartments at the cellular level, as well as on the prominent role played by enzymatic defense systems against PQ poisoning.     

Paraquat resistance in conyza

A biotype of Conyza bonariensis (L.) Cronq. (identical to Conyza linefolia in other publications) originating in Egypt is resistant to the herbicide 1,1′-dimethyl-4,4′-bipyridinium ion (paraquat). Penetration of the cuticle by [¹⁴C]paraquat was greater in the resistant biotype than the susceptible (wild) biotype; therefore, resistance was not due to differences in uptake. The resistant and susceptible biotypes were indistinguishable by measuring in vitro photosystem I partial reactions using paraquat, 6,7-dihydrodipyrido [1,2-α:2′,1′-c] pyrazinediium ion (diquat), or 7,8-dihydro-6H-dipyrido [1,2-α:2′,1′-c] [1,4] diazepinediium ion (triquat) as electron acceptors. Therefore, alteration at the electron acceptor level of photosystem I is not the basis for resistance. Chlorophyll fluorescence measured in vivo was quenched in the susceptible biotype by leaf treatment with the bipyridinium herbicides. Resistance to quenching of in vivo chlorophyll fluorescence was observed in the resistant biotype, indicating that the herbicide was excluded from the chloroplasts. Movement of [¹⁴C] paraquat was restricted in the resistant biotype when excised leaves were supplied [¹⁴C]paraquat through the petiole. We propose that the mechanism of resistance to paraquat is exclusion of paraquat from its site of action in the chloroplast by a rapid sequestration mechanism. No differential binding of paraquat to cell walls isolated from susceptible and resistant biotypes could be detected. The exact site and mechanism of paraquat binding to sequester the herbicide remains to be determined.     

Transition Metals Potentiate Paraquat Toxicity

The involvement of transition metal ions in paraquat toxicity was studied in bacterial model system. We show that the addition of micromolar, or lower, concentrations of copper dramatically enhanced the rate of bacterial inactivation. In contrast, the addition of chelating agents totally eliminated the killing of E. coli. No inactivation was observed under anaerobic exposure to paraquat, both in the absence and presence of copper. However, in the presence of copper, the anaerobic addition of hydrogen peroxide resulted in complete restoration of inactivation as under aerobiosis.

Paraquat either produces superoxide ions or directly reduces bound copper ions in a catalytic mode. The reduced cuprous complexes react with hydrogen peroxide to locally form hydroxyl radicals (OH) which are probably responsible for the deleterious effects.

This study indicates the involvement of a site-specific metal-mediated Haber-Weiss mechanism in paraquat toxicity. It is in agreement with earlier observations that copper unusually enhance biological damage induced by either superoxide or ascorbate.     

Paraquat and iron-dependent lipid peroxidation

The aim of this work was to study the effect of paraquat (P²⁺) on NADPH iron-dependent lipid peroxidation (basal peroxidation) either in the presence of NADPH or in the presence of NADPH-generating systems. When NADPH is present, P²⁺ potentiates NADPH iron-dependent lipid peroxidation, but use of NADPH-generating systems cancels this effect. This may be attributed to certain components in NADPH-generating systems such as glucose-6-phosphate and sodium isocitrate, which act as iron chelators. The binding of iron by these molecules facilitates its reduction and enhances its reactivity toward dioxygen molecules, leading to the formation of reactive species capable of initiating lipid peroxidation, such as Fe³⁺-O ₂ ⁻ . Under these conditions of rapid basal peroxidation, any additional reduction of iron(III) by a reduced form of P²⁺ (P^+.) has no apparent effect on the peroxidation itself, probably because the initial reaction between iron(II) and O₂ followed by initiation of the peroxidation are both rate-limiting steps in the process. Consequently, any alteration of the composition of the reacting mixture (e.g., buffers or the generating system) must be taken into consideration because the formation of new iron chelates can change the rate of basal peroxidation and will modify the effect of redoxcycling molecules.     

Paraquat ingestion and pulmonary injury.

Ventricular aneurysm is usually a complication of acute transmural myocardial infarction. The development of cardiac aneurysm represents a process of continued thinning and fibrosis of the necrotic tissue of the ventricular wall. Survival allows the development of a solid fibrous scar which of itself does not affect global ventricular function substantially. Hence, ventricular aneurysms can be present for up to 18 years without production of serious symptoms. The cases were reviewed of 45 patients in whom aneurysmectomy and myocardial revascularization were carried out. Surgical mortality was low (6.6 percent, 30 days); survival one year after operation was 76 percent, but at three years had fallen to 47 percent. Cause of late death was dominantly cardiac. In 19 patients post-operative study was done; although graft patency was observed in 98 percent, substantive improvement in ventricular performance was seen in a minority of patients. The outcome in patients with ventricular aneurysm is primarily related to the status of the residual myocardium and to the status of the vessels which supply it. The mechanism of clinical improvement after aneurysmectomy has not been clarified. However, the long-term results appear to be similar to those in patients with extensive myocardial infarction.     

Effective Treatment for Paraquat Poisoning in Rats and its Relevance to Treatment of Paraquat Poisoning in Man

After oral administration of a lethal dose of paraquat to rats the plasma concentration remained relatively constant over four to 30 hours and was related to the paraquat content of the small intestine over the first 16 hours. During the first 30 hours the concentration of paraquat in the lung rose progressively above that of the plasma to levels which are known to cause pulmonary damage. A treatment has been devised which prevents the absorption of paraquat into the plasma and prevents accumulation of paraquat in the lung. This treatment consists of a stomach was followed by four administrations of bentonite plus purgatives at two- to three-hour intervals. Even when treatment was delayed until 10 hours after administration of paraquat 80% survival was obtained. The relevance of this treatment to paraquat poisoning in man is discussed in the light of the finding that slices of human lung accumulate paraquat in the same way as those of rat lung.     

腹腔注射百草枯构建小鼠肺纤维化模型

目的:探讨百草枯一次性腹腔注射致小鼠肺纤维化的病理改变及半数致死剂量(LD50),进而制备肺纤维化病理改变稳定的百草枯中毒小鼠肺纤维化模型。方法:60只正常雌性C57BL/6J小鼠被随机分为6组,10只/组,分别为正常对照组及百草枯给药30、40、50、60和80 mg/kg组,所有小鼠于造模后28 d处死,取其左肺用于病理观察(HE染色),并计算LD50及各组肺纤维化Ashcroft评级。结果:至观察期28 d,小鼠一次性腹腔注射百草枯溶液的LD50为55.1923 mg/kg;各染毒组均出现不同程度的肺纤维化改变,且注射剂量越高,肺纤维化病变越严重,但早期死亡率亦越高。结论:一次性腹腔注射百草枯可制备小鼠肺纤维化模型,40和50 mg/kg为较合适的造模剂量。     

Polyamines and Paraquat Toxicity in Arabidopsis thaliana

The relationship between paraquat toxicity and polyamine levelswas analyzed in Arabidopsis wild-type and gi-3 plants. Paraquattreatment led to an increase in putrescine, but not of spermidineand spermine content. Additionally, polyamine feeding offeredhigh levels of protection against paraquat toxicity with spermidinebeing the most effective protectant. (Received March 24, 1998; Accepted June 17, 1998)     

Neurotoxicological Profiling of Paraquat in Zebrafish Model

Neurochemical Research - Paraquat is a polar herbicide protecting plant products against invasive species, it requires careful manipulation and restricted usage because of its harmful potentials....