The investigation of the interaction between 5-Iodouracil and human serum albumin by spectroscopic and modeling methods and determination of protein by synchronous fluorescence technique

The interaction of 5-Iodouracil with human serum albumin (HSA) was investigated in aqueous solution by fluorescence quenching spectrum in combination with UV absorption spectrum and modeling method. The quenching mechanism and binding characteristics of 5-Iodouracil with HSA were obtained from the fluorescence measurement. The binding constants were calculated according to the Lineweaver-Burk equation at different temperatures. And the thermodynamic parameters, enthalpy change (ΔH) and entropy change (ΔS), were calculated by thermodynamic equations. The results showed that the hydrophobic interaction played a major role in the binding of 5-Iodouracil with HSA. The binding distance was obtained according to Föster’s non-radiative energy transfer theory. The effect of some normal ions on the binding constants was discussed. Modeling method was applied to elucidate the interaction mode between 5-Iodouracil and HSA, which was agreed with the calculated result by thermodynamic method. Moreover, the synchronous fluorescence technique was successfully applied to quantify total protein in human body fluids including serum, urine, and saliva samples. The results showed that this method was stable, reliable, selective, sensitive, and practical for the determination of HSA.     

Activation of paraquat in the earthworm Allolobophora chlorotica is mediated by NAD(P)H-cytochrome c reductase activities

This study reports that earthworms, Allolobophora chlorotica, are capable of biotransforming paraquat, a toxic herbicide, resulting in the formation of reactive oxygen species (ROS). We found that in earthworms the reduction of paraquat is mediated by NADPH- and NADH-cytochrome c reductase activities. The formation of superoxide anion (O₂⁻) from the incubation of paraquat with the earthworm extracts was demonstrated by using both Cypridina luciferin analog (CLA) chemiluminescence and the SOD-inhibitable cytochrome c reduction reaction. In addition, in vivo exposure of earthworms to paraquat in solution (24 and 48 h) was performed to investigate whether or not the herbicide affects the levels of the NAD(P)H-cytochrome c reductase activities. Although in vitro NADPH-cytochrome c reductase reduces paraquat more easily than the NADH-dependent activity, after the in vivo exposure an increase of NADH-cytochrome c reductase activity(s) by 12% compared to control values was observed, whereas NADPH-cytochrome c reductase activity was not affected. Xanthine oxidase (XO) is an enzyme implicated in paraquat toxicity, however, no XO was detected in earthworm extracts nor hypoxanthine was a source of electrons for the herbicide reduction. For comparative reasons menadione, a redox cycling quinone, was also incubated with the earthworm extracts. It was found that the incubation of menadione with earthworm extracts formed about two times more (O₂⁻) than with paraquat. It is concluded that the exposure of paraquat to earthworms could elicit radical formation and consequently toxic effects via oxidative stress-mediated mechanisms. The reduction of paraquat by the reductases leads to the formation of paraquat radical, which reacts with molecular oxygen, accounting for the formation of superoxide anion. Further studies are required to conclude that the observed increase of NADH-cytochrome c reductase activity(s) should be used as a biomarker for paraquat exposure in earthworms.     

Pesticides-induced depression of photosynthesis was alleviated by 24-epibrassinolide pretreatment in Cucumis sativus L

The phytotoxicities of nine pesticides (paraquat, fluazifop-p-butyl, haloxyfop, flusilazole, cuproxat, cyazofamid, imidacloprid, chlorpyrifos, and abamectin) at practical dosages on photosynthesis were investigated in cucumber (Cucumis sativus L. cv. Jinyan No. 4) by gas exchange and chlorophyll fluorescent measurements. Plants treated with paraquat showed the severest phytotoxic symptom with the highest reduction in net photosynthetic rate (Pn), while other pesticides except flusilazole inhibited Pn to various degrees. The inhibition of Pn by cuproxat was accompanied by declines both in stomatal conductance (Gs) and intercellular CO₂ concentration (Ci), whereas decreased Pn for the cyazofamid was associated with increased Ci. For other 6 pesticides, however, inhibition of Pn was accompanied by decrease in Gs, while Ci was increased or unaffected. Paraquat almost completely inhibited the maximal quantum efficiency of PSII (F_v/F_m), while other pesticides had no significant effect on F_v/F_m. Quantum efficiency of PSII (Φ_PSII) was significantly reduced by paraquat, fluazifop-p-butyl, and chlorpyrifos and the reduction was mostly attributed to decrease in photochemical quenching coefficient (qP). In comparison, Φ_PSII was not significantly affected by haloxyfop, flusilazole, cyazofamid, imidacloprid, and abamectin. Non-photochemical quenching (NPQ) was suppressed by paraquat and haloxyfop, while apparent upregulation was evident after exposure to other pesticides. Interestedly, inhibitions of Pn were alleviated by 24-epibrassinolide (EBR) pretreatment, as for the pesticides examined in this study except paraquat and flusilazole. EBR pretreatment also increased Φ_PSII and qP. It is likely that EBR enhanced the resistance of cucumber seedlings to pesticides by increasing CO₂ assimilation capacity and activities of antioxidant enzymes.     

Binding of phenthoate to bovine serum albumin and reduced inhibition on acetylcholinesterase

Organophosphorus pesticides (OPs) are of environmental significance due to their high toxicity to animals. Binding to plasma proteins may effective influence the toxicological properties of xenobiotics. In an attempt to evaluate the affinity of phenthoate (PTA) to bovine serum albumin (BSA) and inhibitory ability of bound PTA to acetylcholinesterase (AChE), we investigated the interactions between phenthoate (PTA) and bovine serum albumin (BSA) using tryptophan fluorescence quenching and subsequent inhibition on AChE activity by PTA. The results showed that PTA caused the fluorescence quenching of BSA because of the formation of a PTA-BSA complex. Quenching constants (K_sv), determined using the Sterns-Volmer equation to provide a measure of the binding affinity between PTA and BSA at 303, 306, 310 and 313 K were (3.4295 ± 0.0763) × 10⁻⁴, (3.2446 ± 0.0635) × 10⁻⁴, (3.0434 ± 0.0856) × 10⁻⁴ and (2.8262 ± 0.0569) × 10⁻⁴ M⁻¹, respectively. The thermodynamic parameters, ΔH and ΔS were −25.04 kJ mol⁻¹ and 168.94 J mol⁻¹ K⁻¹, respectively, which indicated that the electrostatic interactions played a major role in PTA-BSA association. The presence of BSA consistently reduced the inhibitory ability of PTA on AChE, with the relative activity being increased from 46.98 to 61.71% for the concentration range of BSA between 0 and 4.0 g L⁻¹.     

Binding of chlorpyrifos and cypermethrin to blood proteins

The features of two insecticides (chlorpyrifos and cypermethrin) binding to two blood proteins, bovine serum albumin (BSA), and bovine hemoglobin (BHb), were investigated via the fluorescence method. The results revealed that both insecticides caused the fluorescence quenching of BSA and the fluorescence enhancement of BHb. A new parameter (F_E), i.e., the fluorescence intensity when adequate insecticide was added, was introduced to obtain the association constant (K_A) and the number of binding sites (n). K_A and n of chlorpyrifos and cypermethrin binding to BSA were 2.99 × 10⁵ and 5.22 × 10⁵ L mol⁻¹, 1.25 and 0.78, respectively. K_A and n of chlorpyrifos and cypermethrin binding to BHb were 2.94 × 10⁴ and 2.48 × 10⁴ L mol⁻¹, 1.75 and 2.19, respectively. In conclusion, chlorpyrifos and cypermethrin could bind to BSA and BHb, and the binding of both insecticides to BSA was significantly stronger than that of insecticides to BHb. These could affect the distribution, metabolism, and excretion of insecticides.     

Leaf tissue pigments and chlorophyll fluorescence parameters vary among sweet corn genotypes of differential herbicide sensitivity

Herbicide applications are meant to eliminate weed competition; however, herbicides may also impose abiotic stress on registered crops. Leaf tissue carotenoid pigments play vital roles in the photoprotection of photosynthetic membranes and contribute to non-photochemical quenching (NPQ) of excitation energy, both important to plant environmental stress tolerance. Our research objectives were to characterize leaf tissue pigments and chlorophyll fluorescence parameters following post-emergence herbicide applications (simulating an abiotic stress) to sweet corn (Zea mays var. rugosa) genotypes of differential herbicide sensitivities. Post-emergence herbicide applications of combinations of mesotrione (105 g ai/ha) and atrazine (560 g ai/ha) were applied to ‘Merit’ (sensitive), ‘Temptation’ (tolerant), and ‘Incredible’ (moderately sensitive) sweet corn genotypes. Leaf tissues were sampled after herbicide applications and measured for chlorophyll fluorescence parameters, and the same tissues were analyzed for carotenoid and chlorophyll pigments. Leaf pigments and chlorophyll fluorescence were not affected by any herbicide treatment; however, data revealed significant differences between genotypes for leaf tissue antheraxanthin, β-carotene, zeaxanthin, chlorophyll a/b ratios, and for values of F_o, F_m, F_v, and NPQ, with ‘Merit’ leaf tissue having higher values than the other two genotypes evaluated. Results demonstrate that genotypic sensitivities to certain post-emergence herbicides may be related to concentrations of photo-protective carotenoids in sweet corn leaf tissues.     

Stress on avocado fruits regulates Δ9-stearoyl ACP desaturase expression,fatty acid composition,antifungal diene level and resistance to Colletotrichum gloeosporioides attack

The expression of the avocado homologue avfad9 encoding Δ⁹-stearoyl-ACP desaturase was enhanced by multiple stimuli: inoculation with Colletotrichum gloeosporioides, exposure to ethylene or CO₂, low temperature (4 °C) and fruit wounding. This enhanced expression was correlated with an increase in the preformed antifungal (Z, Z)-1-acetoxy-2-hydroxy-4-oxo-heneicosa-12,15-diene. Treatments of fruits with ethylene that enhanced the up-regulation of avfad9 also increased the concentration of 18:2 fatty acid and the incorporation of ¹⁴C-linoleate into the antifungal diene. Fruits with enhanced Δ⁹stearoyl-ACP desaturase expression were more resistant to C. gloeosporioides. It is suggested that the enhanced Δ⁹stearoyl-ACP desaturase expression is involved in elevation of unsaturated 18:2. It is also concluded that similar treatments enhance the incorporation of labeled 18:2 into the antifungal diene and elicit the concurrent enhanced resistance to fungal attack.     

Inheritance of resistance to paraquat in barley grass Hordeum glaucum Steud.

Two biotypes of the grass weed barley grass (Hordeum glaucum), one resistant and the other susceptible to the herbicide paraquat, were studied along with their F₁, F₂ and F₃ progeny to determine the inheritance of paraquat resistance. The plants were sprayed with 50–200 g a.i. paraquat ha^?1. These concentrations killed the susceptible type. The data obtained from segregating populations indicated that paraquat resistance in H. glaucum is controlled by a single nuclear gene with incomplete dominance.     

Sclerotinia sclerotiorum catalase SCAT1 affects oxidative stress tolerance,regulates ergosterol levels and controls pathogenic development

Reactive oxygen species (ROS) are essential for pathogenic development of Sclerotinia sclerotiorum. A key question for S. sclerotiorum and many other pathogens concerns how fungi tolerate/dampen the oxidative environment during growth and pathogenesis. Regulatory components of oxidative stress include both enzymatic and non-enzymatic antioxidants. Catalases are a ubiquitous family of enzymes that play an important role in the enzymatic detoxification of ROS by converting hydrogen peroxide (H₂O₂) to water and molecular oxygen. The genome of the omnivorous pathogen S. sclerotiorum contains seven predicted catalase genes. In this study we evaluate and functionally characterize the type A catalase (Scat1) in S. sclerotiorum, whose expression is highly induced during host infection. Insertional inactivation of Scat1 (ΔScat1) resulted in hyperbranching of hyphae accompanied by slower growth and smaller sclerotia. ΔScat1 strains were attenuated in pathogenicity and rendered the fungus hypersensitive to Sodium dodecyl sulfate (SDS), as well as to osmotic and salt stresses. Unexpectedly, ΔScat1 exhibited increased tolerance to H₂O₂, suggesting that although a member of the catalase family, generally associated with amelioration of oxidative stress, Scat1 is probably not required for detoxification of this oxygen species and presumably has different function(s). ΔScat1 strains had a 2-fold decrease in ergosterol content, and overall lower sterol levels compared to the wild-type strain. These observations are consistent with increased resistance to the polyene drugs amphotericin-B and nystatin. Taken together, our results suggest Scat1 is involved in modulation of ROS in a manner that deviates from the detoxification of H₂O₂, alters membrane integrity and contributes to the pathogenic success of S. sclerotiorum.     

Structural and physiological studies of paraquat-resistant Conyza

Structural and physiological studies were conducted with a population of Conyza bonariensis (L.) Cronq. that segregates into paraquat-resistant and -susceptible biotypes. Leaf disks from resistant seedlings, when incubated on 10 μM paraquat for 24 hr, exhibited little difference from the control disks incubated on H₂O as measured by conductivity change, malondialdehyde formation, or plastid ultrastructure. Leaf disks from the susceptible seedlings incubated on 10^?5M paraquat for 24 hr were uniformly bleached, had elevated malondialdehyde content, and leaked more electrolytes than control disks. Plastids of the susceptible biotype incubated on 10^?5M paraquat for 24 hr were swollen organelles with gross rearrangements of the lamella system. Most of the chloroplasts from the central area of the leaf disk of the resistant biotype incubated on a paraquat solution were structurally normal. Swollen plastids and plastids with twisted lamellae were also noted, although much less frequently. Plastids from the edges of the leaf disks of paraquat-resistant clones were structurally similar to those found throughout the leaf disks in susceptible seedlings. When the size of the leaf disk was increased, paraquat-resistant clones exhibited more “resistance” toward paraquat compared to similar-sized leaf disks of the susceptible seedlings. These data are consistent with the hypothesis that the paraquat-resistant seedlings have an altered uptake and/or compartmentalization of paraquat. Superoxide dismutase isozymes, which were previously considered to be related to paraquat resistance in Conyza, did not correlate with the segregation of paraquat resistance in this population.     

Generation of reactive oxygen species by a novel anthraquinone derivative in the cyanobacterium Planktothrix perornata (Skuja)

A water-soluble anthraquinone derivative (2-[methylamino-N-(1′-methylethyl)]-9,10-anthraquinone monophosphate), previously found to be selectively toxic towards Planktothrix perornata at submicromolar concentrations, was studied to determine its toxic mode of action towards this cyanobacterium. Chlorophyll fluorescence was monitored as an indicator of photosynthetic efficiency, and measurement of reactive oxygen species (ROS) was performed using the ROS-sensitive probe 2′,7′-dichlorodihydrofluorescein diacetate. The effects of the herbicide paraquat (a ROS generator) as well as ascorbate and α-tocopherol (ROS scavengers) on ROS formation by P. perornata were studied. Also, the effects of different concentrations of ascorbate, α-tocopherol, and the herbicide diuron on reducing the toxicity of the water-soluble anthraquinone derivative towards P. perornata were determined. Our results indicate that the water-soluble anthraquinone derivative does not inhibit photosynthetic electron transport directly, but does generate ROS at levels that may cause toxicity towards P. perornata.     

Direct measurement of paraquat in leaf protoplasts indicates vacuolar paraquat sequestration as a resistance mechanism in Lolium rigidum

Sequestration of paraquat away from its target site in the chloroplast has been proposed as a mechanism of paraquat resistance. However, no consensus has been reached as to where paraquat is sequestered. This study quantifies paraquat in leaf protoplasts of paraquat resistant (R) and susceptible (S) Lolium rigidum. Intact protoplasts were prepared from plants treated with commercial dose of paraquat for 2 h. Paraquat absorbed by the leaf protoplasts was determined by light absorption of reduced paraquat following concentration and purification using a cation-exchange resin. Leaf protoplasts from treated paraquat resistant plants contained 2- to 3-fold more paraquat than leaf protoplasts isolated from susceptible plants. Since paraquat is not metabolised in L. rigidum and paraquat readily enters chloroplasts of both R and S plants, this greater amount of paraquat in leaf protoplasts of R plant must be kept away from the target site (chloroplast). This result indicates that paraquat resistance in L. rigidum is associated with a cytoplasmic mechanism, most likely a greater rate of vacuolar sequestration.     

人血清白蛋白与氯氰菊酯相互作用的分子模拟研究

运用分子对接、分子动力学、结合自由能计算和丙氨酸扫描等分子模拟方法,研究了人血清白蛋白 (human serum albumin,HSA) 与氯氰菊酯的结合模式。结果表明:氯氰菊酯与HSA结合形成了稳定的复合物,与其氨基酸残基Arg209形成1个氢键,结合自由能为 –83.43 kJ/mol,其中范德华力是结合的主要驱动力,极性溶剂化能是主要抑制力。丙氨酸突变扫描结果显示,氨基酸残基Lys199的ΔΔG_bind值为16.78 kJ/mol,是HSA和氯氰菊酯结合的关键氨基酸。该研究结果为阐明氯氰菊酯在人体内的代谢机制提供了理论参考。     

Inactivation of Paraquat by an Aqueous Extract of Rehmannia glutinosa

Rehmannia glutinosa (Gaertn.) Libosch. ex Fisch. & Mey. was very tolerant to paraquat (1,1′-dimethyl-4,4′-bipyridinium). The paraquat concentration required to reduce dry weight of R. glutinosa by 50% (GR₅₀) was 24 mM , whereas a similar effect was obtained with 0·75 mM in Zea mays L. (maize, cv. Dekalb) and Glycine max (L.) Merr. (soybean, cv. Kwangkyo). When 1·5 mM paraquat in 10% aqueous extract of R. glutinosa was applied to maize and soybean, growth inhibition reached 24% and 7%, respectively, of the untreated control. Decreased activity of paraquat due to the extract also occurred in both leaf discs and chloroplasts of soybean. The total amount of [¹⁴C]paraquat absorbed into soybean leaves after 48 h was 34%, but it was reduced to 17% when the extract was added. Translocation of [¹⁴C]paraquat was also inhibited in the presence of the extract. In thin-layer chromatography (TLC) analysis using various solvent systems, R_f values of [¹⁴C]paraquat with the extract differed from those without the extract. The results suggested that the aqueous extract of R. glutinosa contained a substance which could nullify paraquat activity. © 1997 SCI.     

Binding of mercury compounds to the chloroplasts in relation to the inhibition of the Hill reaction

The binding behavior of mercuric chloride (HgCl₂), phenylmercuric acetate (PMA), and ethylmercuric chloride (EMC) to the spinach chloroplasts in relation to the inhibition of the Hill reaction was studied at pH 6.8 and 7.8 using ²⁰³Hg labeled compounds. The pH of the reaction medium did not influence the amount of mercury binding of the chloroplast at various mercurial concentrations, but it altered the inhibition curve of the Hill reaction. Between 0–1 × 10^?5M the binding of Hg²⁺ and EMC were similar and increased linearly with the concentration, while the binding of PMA was similar to the binding of Hg²⁺ only at a concentration below 4 × 10^?6M and was less when the concentration was above 4 × 10^?6M. However, the inhibition of the Hill reaction by these mercury compounds was quite different; at pH 7.8, the I₅₀ values for Hg²⁺, PMA, and EMC were 5 × 10^?6, 2.5 × 10^?6, and 2.5 × 10^?6M, respectively, while at pH 6.8, these values were 4 × 10^?6, 4 × 10^?5, and 2 × 10^?4M, respectively. The differential block of electron flow by the mercury compounds at pH 6.8 and 7.8 was further confirmed by electron spin resonance study.     

小麦抗白粉病基因Pm2的SSR标记筛选

为筛选与小麦抗白粉病基因Pm2紧密连锁的分子标记,将感病品种Chancellor与Pm2的近等基因系杂交,获得F1、F2分离群体,采用分离群体分组法对Pm2进行了微卫星(microsatellite,又称simple sequence repeats,SSR)标记分析.结果表明,定位于小麦5D染色体上的71对SSR引物中有12对引物能在Pm2的近等基因系、Chancellor间稳定地揭示出多态性差异,7对引物Xcfd189、Xcfd29、Xcfd8、Xcfd102、Xcfd7、Xcfd57和Xgwm190分别能在抗病、感病池间和F2分离群体的抗病、感病单株间稳定地扩增出特异性产物.7对引物所扩增的特异谱带分别为:Xcfd189360、Xcfd29190、Xcfd8160、Xcfd102250、Xcfd7200、Xcfd57245和Xgwm190210,它们与Pm2基因间的遗传距离分别为0、1.5、2.3、5.4、10.2、31.5和54.3 cM,其中标记Xcfd189360与Pm2共分离,标记Xcfd29190、Xcfd8160和Xcfd102250与Pm2紧密连锁,可用于Pm2的标记辅助选择.     

Protective effect of dimercaptosuccinic acid on methylmercury and mercuric chloride inhibition of rat brain muscarinic acetylcholine receptors

The reactivation of the rat brain muscarinic acetylcholine receptor (mACh-R) binding with dimercaptosuccinic acid (DMSA) after in vitro and in vivo inhibition by mercuric chloride (HgCl₂) and methylmercuric chloride (MeHg) was investigated. Receptor binding was estimated by the potent and specific antagonist l-[³H]quinuclidinyl benzilate ([³H]QNB). Rat brain synaptosomal membranes were exposed to HgCl₂ and MeHg. At 1 × 10^?4M. HgCl₂ caused complete inhibition of the [³H]QNB binding. The inhibition of [³H]QNB binding by HgCl₂ was still higher than 50% at 1 × 10^?8M. MeHg caused less inhibition of [³H]QNB binding than HgCl₂. The inhibited receptors showed a significant degree of reactivation when treated with DMSA. The recovery was almost complete after MeHg inhibition or with the lower HgCl₂ concentrations. Generally, the reactivation was dependent on the concentration of DMSA. When rats injected with either early or delayed doses of DMSA following administration with five consecutive daily doses (8 mg/kg body wt, Gavage method) of MeHg or HgCl₂, the inhibition of [³H]QNB binding was less than untreated ones. The early treatment with DMSA decreased the inhibition of [³H]QNB binding due to MeHg or HgCl₂ intoxication. However, DMSA was more effective in reducing HgCl₂ inhibition than MeHg either in vitro or in vivo treatment. The ability of DMSA to reactivate the mACh-R after inhibition with the mercurials emphasizes the involvement of essential sulfhydryl groups in [³H]QNB binding sites, and also shows that these sulfhydryl groups are the primary target for the MeHg and HgCl₂ inhibition of the rat brain muscarinic receptors.     

Effect of miconazole,an antifungal agent,on allene oxide synthase: Inhibition,kinetics, and binding

We investigated the inhibition of allene oxide synthase (AOS), a key enzyme in jasmonic acid biosynthesis, by miconazole. Kinetic analysis indicated that miconazole was a mixed-type inhibitor of AOS with a K_i value of approximately 8.4 ± 0.2 μM. Analysis of the interactions between miconazole and AOS by optical difference spectroscopy revealed that miconazole binding induces type II binding spectra with a K_d value of approximately 6.0 ± 0.2 μM.     

Effects of insecticide acetamiprid on photosystem II (PSII) activity of Synechocystis sp. (FACHB-898)

Effects of insecticide acetamiprid on photosystem II (PSII) activity of Synechocystis sp. were investigated by a variety of in vivo chlorophyll fluorescence tests. Acetamiprid exposure increased the proportion of inactivated PSII reactive centers (PSII_X) and led to loss of active centers (PSII_A). High concentration (1.0 mM) acetamiprid decreased amplitude of the fast phase and increased the slow phase of fluorescence decay during reoxidation. The electron transport after Q_A was hindered by high concentration acetamiprid and more Q_A had to be reoxidized through S₂(Q_AQ_B)⁻ charge recombination. Acetamiprid decreased the density of the active reaction centers, electron transport flux per cross section and the performance of PSII activity but had little effect on dissipated energy flux per reaction center, antenna size and the maximum quantum yield for primary photochemistry (F_v/F_m). The target site of acetamiprid toxicity to the PSII of Synechocystis sp. was electron transfer on the acceptor side.     

Reduced paraquat translocation in paraquat resistant Arctotheca calendula (L.) Levyns is a consequence of the primary resistance mechanism, not the cause

Resistance to paraquat has been studied in detail in many weed species for more than a decade, with the precise mechanism of resistance still unclear. Several studies have indicated that reduced movement of the herbicide to the site of action in the chloroplast is at least partly responsible for endowing resistance. Although paraquat translocation studies have been performed in the past it has been rare for these studies to have been conducted on whole plants in the light, despite early observations which clearly showed that paraquat translocation is minimal unless treated plants are exposed to light. This study has addressed this issue in Arctotheca calendula by tracing the movement of ¹⁴C-paraquat in resistant and susceptible plants in both the dark and light. Differences in paraquat translocation between the resistant and susceptible biotypes of A. calendula were only observed when treated plants were exposed to light. It was observed that paraquat translocation was significantly reduced in the resistant compared to the susceptible biotype when plants were exposed to light but not in the dark. It is postulated that paraquat translocation is dependent on light mediated damage. As paraquat-induced damage is less severe in paraquat resistant plants, overall paraquat translocation is reduced in the resistant biotype.