Differential effects of phenoxy herbicides on light-dependent 14CO2 fixation in isolated cells of C3 and C4 plants

Cells were isolated from the developing leaves of Ipomoea aquatica and Digitaria sanguinalis. The effects of phenoxy alkanoic acid herbicides on light-dependent ¹⁴CO₂ fixation and oxygen evolution in these leaf cells were studied. (2,4-Dichlorophenoxy)acetic acid and (2,4,5-trichlorophenoxy) acetic acid (2,4,5-T and 2,4-D) caused a 20% stimulation of ¹⁴CO₂ fixation at 0.8 × 10^?5M and an inhibition at 1 × 10^?4M in I. aquatica leaf cells. Temperature seemed to have a marked influence on such action. No effect or very little effect was observed in the leaf cells of D. sanguinalis. The nonactive (2,4,6-Trichlorophenoxy)acetic acid (2,4,6-T) caused a similar stimulation of CO₂ fixation as 2,4-D and 2,4,5-T at low concentrations in I. aquatica leaf cells, but no inhibition was observed at high concentration. Increase of hight intensity increased the rate of CO₂ fixation in both control and 2,4,6-T-treated cells; however, the percentage of stimulation remained the same. At stimulatory concentration, all three compounds did not cause any stimulation in either photosystem I and II or photosystem II-mediated oxygen evolution. At higher concentrations, the differential effects of 2,4-D and 2,4,5-T on the light-induced CO₂ fixation and photosystem II-mediated oxygen evolution in the I. aquatica leaf cells and D. sanguinalis mesophyll (ms) cells may be attributed in part to their selective action against dicotyledonous plants.     

Comparative metabolism of 1,1-Bis-(p-chlorophenyl)-2-nitropropane (Prolan) in mouse,insects, and in a model ecosystem

¹⁴C-labeled Prolan or 1,1-bis-(p-chlorophenyl)-2-nitropropane was found to be some-what more biodegradable than DDT. This insecticide, although highly resistant to microsomal metabolism, was degraded by elimination to 1,1-bis-(p-chlorophenyl)-1-propene, and by reduction to 1,1-bis-(p-chlorophenyl)-2-aminopropane. The major degradative pathway, however, was by oxidation to 1,1-bis-(p-chlorophenyl)-2-propanone, to 1,1-bis-(p-chlorophenyl)-pyruvic acid, to bis-(p-chlorophenyl)-acetic acid, and ultimately to p,p′-dichlorobenzophenone. Therefore the ultimate degradative products of Prolan are identical to those produced from DDT.     

Effect of chlorfenprop-methyl, flamprop-isopropyl and benzoylprop-ethyl on 14C2 fixation in Avena fatua L., Triticum aestivum L. and Hordeum vulgare L.

The effect of chlorfenprop-methyl, flampropisopropyl and benzoylprop-ethyl on ¹⁴CO₂ fixation was followed in wild oat (Avena fatua L.), barley (Hordeum vulgare L., cv. Ametyst), and wheat (Triticum aestivum L., cv. Mironovská). Experimental plants were exposed to a ¹⁴CO₂-enriched atmosphere in a special apparatus 2 h, 1, 3, and 9 days after the herbicide treatment. Chlorfenprop-methyl already inhibited ¹⁴CO₂ fixation in wild oat plants 2 h after the treatment. ¹⁴C-metabolite transport to the roots was strongly decreased. Both ¹⁴CO₂ fixation and ¹⁴C-metabolite level in the roots were significantly depressed in A. fatua when compared with untreated plants at the last sampling time. ¹⁴C incorporation into starch was inhibited from the first day after treatment, and on day 9 was lowered more than ten fold in treated plants. Flamprop-isopropyl inhibited ¹⁴CO₂ fixation in wild oat plants from day 3 after treatment, but benzoylprop-ethyl not until day 9. Both herbicides also decreased ¹⁴C incorporation into starch in A. fatua. Chlorfenprop-methyl also slightly decreased ¹⁴CO₂ fixation in barley on day 9. However, assimilate transport into the roots and ¹⁴C incorporation into starch were not affected. Flamprop-isopropyl inhibited ¹⁴CO₂ fixation in barley plants only on the first day after treatment, and assimilate transport was also reduced. By contrast, no differences from untreated plants were found at the end of the experiment. Benzoylprop-ethyl did not decrease either ¹⁴CO2 fixation or assimilate transport to the roots in wheat, but it inhibited starch synthesis. Atrazine depressed ¹⁴CO₂ fixation in wild oat plants by 91%, in wheat plants by 99% compared with untreated plants. Assimilate transport into the roots was also strongly inhibited. In contrast to atrazine, the effect of chlorfenprop-methyl, flamprop-isopropyl, and benzoylprop-ethyl on CO₂ fixation seems to be secondary.     

Influence of monuron on photosystem II and light-dependent 14CO2 fixation in isolated cells of C3 and C4 plants

Cells were isolated from the developing leaves of Ipomoea aquatica (water spinach), a C₃ plant, and three kinds of C₄ plants, namely, Digitaria sanguinalis (NADP⁺-specific malate dehydrogenase type), Panicum miliaceum (NAD⁺-specific malic enzyme type), and Panicum texanum (phosphoenopyruvate carboxy kinase type), to study the effect of monuron on light-dependent ¹⁴CO₂ fixation and oxygen evolution. Bundle sheath cells, except for those of D. sanguinalis, and mesophyll cells of all plants fixed approximately the same amount of ¹⁴CO₂. Monuron, at the range used (2 to 10 × 10^?7M), showed strong inhibition in the mesophyll cells of water spinach and in bundle sheath cells of P. miliaceum and P. texanum and moderate inhibition in the mesophyll cells of all C₄ plants. In the bundle sheath cells of D. sanguinalis the low rate of ¹⁴CO₂ fixation was stimulated to some extent by the addition of malate and ribose 5-phosphate. The I₅₀ value was 6 × 10^?7M for the sensitive cells. Monuron inhibited the oxygen evolution of all seven cell types and their I₅₀ values varied between 3 × 10^?7 to 6 × 10^?7M. The differential response of isolated plant cells from different species to light-dependent CO₂ fixation in the presence of monuron may also be involved in urea herbicide selectivity and undoubtedly is due to the differential photosynthetic pathways present nn them.     

Degradation of fluometuron by Rhizoctonia solani

Degradation studies of fluometuron [Cotoran, 1,1-dimethyl-3-(α,α,α-trifluoro-m-tolyl)urea] by Rhizoctonia solani have been conducted to elucidate further the pathway of degradation. Analysis by thin-layer chromatography and autoradiography demonstrated that R. solani degraded 88% of fluometuron (¹⁴CF_3^?) into seven nonpolar metabolites after 35 days of incubation. Trace amounts of polar, water-soluble products were detected, but no ¹⁴CO₂ or radioactive volatile products were detected. Two of the major metabolites were identified by thin-layer chromatography and ultraviolet spectroscopy as 1-methyl-3-(α,α,α-trifluorotolyl)urea and (3-trifluoromethylphenyl)urea, which indicated a stepwise demethylation of fluometuron. The remaining five metabolites have not been identified and have not been previously reported in the literature. Time course experiments and metabolite degradative studies indicated that the sequence of degradation involved a multibranched pathway which did not include CO₂ evolution. The proposed pathway does not include the conversion of fluometuron to the aniline derivative as has been reported for other urea herbicides. All of the data from this study indicate the incomplete degradation of fluometuron which suggests a cometabolic degradative pathway.     

Studies on effects of certain quinones: III. Photosynthetic 14CO2 incorporation by Rhodospirillum rubrum

Substituted naphthoquinones, 2,3,-dichloro-1,4-naphthoquinone, and 2-methyl-1,4-naphthoquinone produced marked changes in the pattern of ¹⁴C-distribution during ¹⁴CO₂-fixation by photosynthetic bacterium Rhodospirillum rubrum. The most obvious change in the labeling pattern during photoautotrophic ¹⁴CO₂-fixation was a several-fold increase in 3-phosphoglyceric acid accompanied with a decrease in the amount of glutamate. In photoheterotrophic cells, quinones caused an appreciable increase in ¹⁴C-glycolic acid and concomitant decrease, although not proportional, in the amount of ¹⁴C-sugar phosphate. The level of ¹⁴C-incorporated in poly-β-hydroxybutyrate and ether-extractable lipids was considerably decreased in photoautotrophic and photoheterotrophic cells treated with quinones. The ability of quinones to interfere with the synthesis of NADH and ATP, and their ability to interact with sulfhydryl enzymes and coenzymes appears to be responsible for the changes observed.     

Differential effects of phenoxy herbicides on light-dependent CO2 fixation in isolated cells of C3 and C4 plants

Cells were isolated from the developing leaves of Ipomoea aquatica and Digitaria sanguinalis. The effects of phenoxy alkanoic acid herbicides on light-dependent ¹⁴CO₂ fixation and oxygen evolution in these leaf cells were studied. (2,4-Dichlorophenoxy)acetic acid and (2,4,5-trichlorophenoxy) acetic acid (2,4,5-T and 2,4-D) caused a 20% stimulation of ¹⁴CO₂ fixation at 0.8 × 10⁻⁵M and an inhibition at 1 × 10⁻⁴M in I. aquatica leaf cells. Temperature seemed to have a marked influence on such action. No effect or very little effect was observed in the leaf cells of D. sanguinalis. The nonactive (2,4,6-Trichlorophenoxy)acetic acid (2,4,6-T) caused a similar stimulation of CO₂ fixation as 2,4-D and 2,4,5-T at low concentrations in I. aquatica leaf cells, but no inhibition was observed at high concentration. Increase of hight intensity increased the rate of CO₂ fixation in both control and 2,4,6-T-treated cells; however, the percentage of stimulation remained the same. At stimulatory concentration, all three compounds did not cause any stimulation in either photosystem I and II or photosystem II-mediated oxygen evolution. At higher concentrations, the differential effects of 2,4-D and 2,4,5-T on the light-induced CO₂ fixation and photosystem II-mediated oxygen evolution in the I. aquatica leaf cells and D. sanguinalis mesophyll (ms) cells may be attributed in part to their selective action against dicotyledonous plants.     

Degradation of ioxynil to CO2 in soil

Degradation of ioxynil (4-hydroxy-3,5-diiodobenzonitrile) to CO₂ was detected in a clay loam, high organic matter content soil. The majority of radioactivity was recovered as ¹⁴CO₂ from both ring-labeled and cyano-labeled ioxynil; however, ¹⁴CO₂ was always released from cyano-labeled ioxynil at a much faster initial rate. No ¹⁴CO₂ was released in treated sterile soil, either aerobically or anaerobically. Production of ¹⁴CO₂ from cyanolabeled and ring-labeled ioxynil was greatly inhibited by HgCl₂ (10^?5M), and p-chloromercuribenzoate (5 × 10^?5M), but slightly inhibited by ferricyanide (10^?4M). No ¹⁴CO₂ was evolved from ring-labeled ioxynil under anaerobic conditions. These observations indicated that the degradation of ioxynil to CO₂ in soil was a microbial action and was oxygen dependent. This is consistent with the known mechanism of oxygenases in degrading benzene rings. Anaerobically, a small amount of ¹⁴CO₂ was released from cyano-labeled ioxynil. Thin-layer chromatographic analyses of the culture supernatant revealed that 3,5-diiodo-4-hydroxybenzamide and 3,5-diiodo-4-hydroxybenzoic acid were intermediate metabolites.     

Effect of liver enzyme induction on paraoxon metabolism in the rat

Orally administered [1-¹⁴C]ethyl paraoxon, O,O-diethyl-O-p-nitrophenyl phosphate, is readily absorbed from the gastrointestinal tract of male albino rats. Radioactivity is essentially eliminated in 72 hr by excretion into urine and feces and by expiration as ¹⁴CO₂. Compounds with radioactivity in the urine are tentatively identified as diethyl phosphoric acid, desethyl paraoxon, ethanol, metabolites conjugated with amino acids, and paraoxon; the first compound is the predominant radioactive metabolite. Intraperitoneally injected phenobarbital, DDT, dieldrin, and endrin are inducers of microsomal enzymes that degrade paraoxon. The aryl phosphate-cleaving activity in vitro is not dependent on the addition of NADPH. O-Dealkylation of paraoxon is catalyzed by microsomal enzymes that require NADPH and oxygen and are inhibited by carbon monoxide. Microsomal enzymes from rats pretreated with enzyme inducers give an increased rate of O-dealkylation of paraoxon. Reduced glutathione has little or no effect on paraoxon degradation by either microsomal or soluble enzymes. Actinomycin D inhibits O-dealkylation of paraoxon in vivo, as indicated by reduction of ¹⁴CO₂ formation, and in vitro, as indicated by decreased activity of microsomal O-dealkylase. The role of microsomal mixed-function oxidases and NADPH-dependent O-dealkylase in the metabolism of organophosphorus insecticides is discussed.     

Glyphosate uncouples gas exchange and chlorophyll fluorescence

BACKGROUND: Changes in chlorophyll fluorescence have often been advocated as a sensitive biomarker of plant stress, assuming that any kind of plant stress serious enough to affect plant growth will also affect photosynthesis. Glyphosate affects photosynthetic electron transport indirectly by inhibiting sink processes. The question is how fast this inhibition can be observed on CO₂ assimilation and ultimately on chlorophyll fluorescence? RESULTS: Experiments measuring CO₂ assimilation, conductance and chlorophyll fluorescence using four Kautsky curve parameters on barley (Hordeum vulgare L.) exposed to increasing doses of glyphosate showed a total cessation of CO₂ fixation and conductance without significant changes in chlorophyll fluorescence. The decrease in CO₂ fixation and conductance was significant 1 day after spraying and corresponded well to the decrease in biomass 5–7 days after spraying. CONCLUSION: A total cessation of CO₂ assimilation can take place without affecting chlorophyll fluorescence. Hypotheses concerning what happens to the energy from the photosynthetic apparatus that is not used for CO₂ assimilation are discussed. The results question the use of chlorophyll fluorescence as a universal indicator of stress on photosynthetic processes. Also, they demonstrate that changes in gas‐exchange parameters are more sensitive biomarkers for glyphosate toxicity compared with chlorophyll fluorescence. Copyright © 2010 Society of Chemical Industry     

DDT and pyrethroids: Receptor binding and mode of action in the house fly

The mode of action of DDT and pyrethroids was investigated in the house fly, Musca domestica L, using drug:receptor binding techniques. Both in vivo and in vitro binding studies demonstrated the existence of membrane receptors which bind specifically to [¹⁴C]DDT and [¹⁴C]cis-permethrin. The receptors show properties to be expected of a critical target site of these insecticides. These include negative temperature correlation with binding, relatively nonsensitivity to DDE, and sensitivity to Ca²⁺. The receptor sites are readily saturated at 45–90 nM [¹⁴C]DDT and have an apparent disassociation constant (K_d) of 12.2 nM. The maximum number of binding sites was estimated to be 17 pmol DDT/mg membrane protein (0.34 pmol/house fly head). Competition studies showed DDT, cis-permethrin, and cypermethrin bind to the same receptor but not at precisely the same site. The addition of Ca²⁺ to the incubation buffer significantly inhibited the binding of both [¹⁴C]DDT and [¹⁴C]cis-permethrin, suggesting the receptor binding is Ca²⁺ sensitive and may have a role in ion conductance.     

Metabolism of O,O,S-trimethyl phosphorothioate in rats after oral administration of a toxic dose,and the effect of coadministration of its antagonistic thionate isomer

The in vivo metabolism of [¹⁴CH₃S]- and [¹⁴CH₃O]O,O,S-trimethyl phosphorothioate (OOS) was followed in rats after oral administration of threshold or LD₅₀ toxic doses of 20 or 60 mg/kg. Similar metabolic studies were conducted with coadministration of 1% O,O,O-trimethyl phosphorothionate (OOO), which prevented all signs of delayed toxicity, including weight loss. When administered alone, OOS was metabolized mainly (50–60%) via removal of the CH₃S moiety, which was largely converted to expired CO₂. Approximately 20% of the compound was O-demethylated, presumably by conjugation with glutathione, and then further metabolized to CO₂. Major urinary products were identified as O,O-dimethyl phosphoric acid (50–60%) and O,S-dimethyl phosphorothioic acid (～20%). Coadministration of OOO caused a slight decrease (～5%) in the cleavage of the CH₃S moiety, indicated by a reduction in ¹⁴CO₂ from [¹⁴CH₃S]OOS and a quantitatively similar increase in the formation of O,S-dimethyl phosphoric acid. Limited pharmacokinetic studies indicated that OOS was rapidly absorbed and distributed throughout the body. Coadministration of 1% OOO caused a slight increase in the blood half-life of parent OOS when administered at 60 mg/kg. It was concluded that a small proportion of the cleavage of the CH₃S moiety from OOS is involved in the intoxication process, and that this intoxication reaction is specifically inhibited by OOO.     

Growth, photosynthetic pigments and photosynthetic activity during seedling stage of cowpea (Vigna unguiculata) in response to UV-B and dimethoate

UV-B (0.4 W m⁻²) irradiation and dimethoate (100 and 200 ppm) treatments, singly and in combination, declined the growth, photosynthetic pigment contents and photosynthesis (O₂ evolution and CO₂-fixation) of cowpea (Vigna unguiculata). Contrary to this, low concentration of dimethoate (50 ppm) caused stimulation on these parameters, while together with UV-B it showed inhibitory effects. Carotenoids (Car) showed varied responses. It was found that carbon-fixation (¹⁴CO₂) was more sensitive to both the stresses than photosynthetic oxygen evolution. Photosynthetic electron transport activity was reduced by both the stresses, however, 50 ppm dimethoate besides inhibiting photosystem II (PSII) and whole chain activity, showed slight stimulation in photosystem I (PSI) activity. The individual effect of two stresses on PSII activity was probably due to interruption of electron flow at oxidation side of PSII which extended to its reaction center following simultaneous exposure. A similar trend was also noticed in case of CO₂ liberation (measured as ¹⁴CO₂ release) in light and dark. Results suggest that dimethoate (100 and 200 ppm) and UV-B alone caused heavy damage on pigments and photosynthetic activity of cowpea, leading to the significant inhibition in growth. Further, the interactive effects of both the stresses got intensified. However, low concentration (50 ppm) of dimethoate showed stimulation, but in combination, it slightly recovered from the damaging effect, caused by UV-B.     

DDT and pyrethroids: Receptor binding in relation to knockdown resistance (kdr) in the house fly

The nature of target site or knockdown resistance (kdr) to DDT and pyrethroids was studied by investigating specific binding of [14_C] DDT and [14_C] cis-permethrin to the previously established membrane receptors from the heads of susceptible (sbo) and resistant (kdr) strains of the house fly, Musca domestica L. In vivo studies showed the heads from sbo flies bound two to three times more DDT than those from kdr flies at all doses tested. Reduced binding was also observed in kdr flies in in vitro [14_C] DDT binding assays. Scatchard analysis indicated that kdr flies have the same affinity but fewer receptors per milligram protein in the CNS than sbo flies. Assays with [14_C] cis-permethrin also showed binding was much reduced in kdr flies in comparison with sbo flies. Based on these results, the nature of the target site insensitivity of kdr flies may relate to their having a reduced number of receptors for the insecticides.     

Influence of the herbicides hexazinone and chlorsulfuron on the metabolism of isolated soybean leaf cells

The effects of the herbicides hexazinone [3-cyclohexyl-6-(dimethylamino)-1-methyl-1,3,5-triazine-2,4(1H,3H)-dione] and chlorsulfuron (2-chloro-N-[(4-methoxy-6-methyl-1,3,5-triazin-2-yl)aminocarbonyl]benzenesulfonamide) on the metabolism of enzymatically isolated leaf cells from soybean [Glycine max (L.) Merr., cv. ‘Essex’] were examined. Photosynthesis, protein, ribonucleic acid (RNA), and lipid syntheses were assayed by the incorporation of specific radioactive substrates into the isolated soybean leaf cells. These specific substrates were NaH¹⁴CO₃, [¹⁴C]leucine, [¹⁴C]uracil, and [¹⁴C]acetate, respectively. Time-course and concentration studies included incubation periods of 30, 60, and 120 min and concentrations of 0.1, 1, 10, and 100 μM of both herbicides. Photosynthesis was the most sensitive and first metabolic process inhibited by hexazinone. RNA and lipid syntheses were also inhibited significantly by hexazinone whereas the effect of this herbicide on protein synthesis was less. The most sensitive and first metabolic process inhibited by chlorsulfuron was lipid synthesis. Photosynthesis, RNA, and protein syntheses were affected significantly only by the highest concentration of this herbicide and longest exposure. Although these two herbicides may exert their herbicidal action by affecting other plant metabolic processes not examined in this study, hexazinone appears to be a strong photosynthetic inhibitor, while the herbicidal action of chlorsulfuron appeared to be related to its effects on lipid synthesis.     

Degradation of the pyrethroid insecticide WL 41706, (±)-α-cyano-3-phenoxybenzyl 2,2,3,3-tetramethylcyclopropanecarboxylate,in soils

The degradation of the insecticide WL 41706, (±)-α-cyano-3-phenoxybenzyl 2,2,3,3-tetramethylcyclopropanecarboxylate, (I), in two soils from Spain and one from the UK has been studied in the laboratory. Samples of (I) labelled separately with ¹⁴C in the benzyl ring (uniform labelling) and at C₍₁₎ of the cyclopropyl ring were used. The insecticide underwent degradation by hydrolysis at the cyano group to form the amide and carboxylic acid analogues. However, the major degradative route was hydrolysis at the ester linkage leading initially to the formation of 3-phenoxy-benzoic acid and 2,2,3,3-tetramethylcyclopropanecarboxylic acid. When a sandy clay soil was treated with [benzyl^?14C]-WL 41706 under balance conditions, ¹⁴CO₂ was evolved at a steady rate and 16 % of the applied radiolabel was detected as ¹⁴CO₂ over a 26 week period. The rate of degradation of I was most rapid on a moist sandy clay (loss of 50 % initial quantity in 4 weeks) but it was considerably slower on dry sandy clay and moist clay soils (> 16 weeks). Under flooded, anaerobic conditions the rate of hydrolysis of the insecticide was slower than under aerobic conditions and the 3-phenoxybenzoic acid and 2,2,3,3-tetramethylcyclopropanecarboxylic acid were found to accumulate over the 24 weeks of the experiment.     

The distribution and degradation of chlormequat in wheat plants

The distribution and degradation of chlormequat chloride (2-chloro 1,2-¹⁴C ethyltrimethylammonium chloride) was determined after uptake by the roots of summer wheat seedlings. This plant regulator was readily translocated from the roots to the above ground parts and converted into choline. Choline was further metabolized to betaine which upon demethylation yielded finally glycine and serine. Both amino acids were incorporated into a protein fraction.The occurrence of radioactively labeled glycine and serine in the amino acid pool and the evolution of ¹⁴CO₂ from chlormequat treated plants indicated that serine was formed from glycine under the release of ¹⁴CO₂ during photorespiration.One week after the uptake period 82% of ¹⁴C chlormequat taken up by the roots was recovered as the parent compound or as breakdown products in wheat plants. In addition 5% of the amount taken up by the roots was released as ¹⁴CO₂ by the leaves.Fifty per cent of the total amount of chlormequat originally present in roots and leaves was already metabolized after 7.5 days. No evidence has been obtained for the presence of unchanged chlormequat or an unknown metabolite in the nucleic acid or protein fraction.     

Studies on the mechanism of estrogenic actions of o,p′DDT: Interactions with the estrogen receptor

The ability of o,p′DDT to bind to the 8S moiety in the uterine cytosol or to interfere with the binding of ³H-estradiol-17β (³H-E₂) to that binding component was investigated utilizing a 10–30% sucrose gradient sedimentation analysis. Attempts to demonstrate the binding of radiolabeled o,p′DDT to the 8S receptor in the mouse and rabbit were not successful, presumably due to the relatively low specific activity of the radiolabeled o,p′DDT, however, binding to the “nonspecific” 4S site(s) was detected. On the other hand, the addition of nonlabeled o,p′DDT inhibited the binding of ³H-E₂ to the 8S receptor. Thus, o,p′DDT (2 μM) suppressed by 58% the binding of ³H-E₂ (2 nM) in the 8S region in ovariectomized adult mice. Similarly, in immature rats three concentrations of o,p′DDT (16, 32, and 96 μM) inhibited by 39.5, 52.9, and 59.7% respectively, the binding of ³H-E₂ (2.8 nM). Similar results were obtained with uterine preparations from mature rats. However, the suppression of binding of ³H-E₂ in the 8S region resulted in an increased binding in the 3–4S region.A Scatchard plot analysis of the binding of ³H-E₂ in the presence of o,p′DDT revealed the same number of binding sites as in the absence of o,p′DDT, indicating that o,p′DDT did not “destroy” the binding capacity. Also, this analysis revealed that o,p′DDT merely caused a decrease in the ratio of the bound to free E₂, indicating that o,p′DDT binds to the receptor and thus interferes with E₂ binding.In addition, our observations that the administration of o,p′DDT to immature female rats causes a marked increase in the levels of the uterine nuclear binding sites (nuclear estogren receptor) is a further indication that o,p′DDT acts as a typical estrogenic compound. However, whether o,p′DDT has antiestrogenic activity as well has not been established.     

Effect of certain substituted naphthoquinones on growth and respiration of Rhodospirillum rubrum

The effect of dichlone (2,3-dichloro-1,4-naphthoquinone) on photoautotrophic, photoheterotrophic and heterotrophic growth, and respiration of Rhodospirillum rubrum (a nonsulfur purple bacterium) was studied to elucidate the mechanism of action of this toxicant on photosynthetic bacteria. The photosynthetic growth with malate or with hydrogen and CO₂ was inhibited by dichlone. Light respiration of photoheterotrophically grown cells, unlike their dark respiration, was found to be insensitive to dichlone. Although dichlone caused an inhibition of the respiration of dark-grown cells, such cells were able to grow in the presence of dichlone after a lag. Light-dependent ¹⁴C-substrate incorporation by photoheterotrophic or photoautotrophic cells was found to be relatively more sensitive to dichlone than oxidative substrate incorporation by heterotrophic cells. Short-term exposure of the light-grown cells to dichlone resulted in an irreparable loss of their ability to grow photosynthetically and photoassimilate ¹⁴C-substrates. Menadione (2-methyl-1,4-naphthoquinone), a synthetic vitamin K, failed to affect these reactions to a significant extent at comparable concentrations. The findings suggest that dichlone causes an irreversible damage to some primary photosynthetic reaction in chromatophores, whereas the damage caused to the dark heterotrophic metabolism of the cell is less severe and repairable. The inhibitory action of dichlone does not appear to be via the formation of semiquinone free radicals.