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PubMed2006

Effect of Saffron (Crocus sativus) on neurobehavioral and neurochemical changes in cerebral ischemia in rats.

The modifying effects of Crocus sativus (CS) stigma extract on neurobehavioral activities, malondialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase, glutathione reductase, glutathione S-transferase, superoxide dismutase (SOD), catalase (CAT), and Na(+),K(+)-ATPase activities, and glutamate (Glu) and aspartate (Asp) content were examined in the middle cerebral artery (MCA) occlusion (MCAO) model of acute cerebral ischemia in rats. The right MCA of male Wistar rats was occluded for 2 hours using intraluminal 4-0 monofilament, and reperfusion was allowed for 22 hours. MCAO caused significant depletion in the contents of GSH and its dependent enzymes while significant elevation of MDA, Glu, and Asp. The activities of Na(+),K(+)-ATPase, SOD, and CAT were decreased significantly by MCAO. The neurobehavioral activities (grip strength, spontaneous motor activity, and motor coordination) were also decreased significantly in the MCAO group. All the alterations induced by ischemia were significantly attenuated by pretreatment of CS (100 mg/kg of body weight, p.o.) 7 days before the induction of MCAO and correlated well with histopathology by decreasing the neuronal cell death following MCAO and reperfusion. The present results may suggest the effectiveness of CS in focal ischemia most probably by virtue of its antioxidant property.

Animals↗

PubMed1999

Risk assessment of cardiovascular diseases among bank employees--a biochemical approach.

In different epidemiological studies, an association between sedentary life style and incidence of cardiovascular diseases has been demonstrated. This study was carried out among 50 sedentary bank employees working at different nationalized banks within Calcutta City, India and 50 individuals with non-sedentary jobs matched for age group and sex for the control group. Body mass index (BMI), blood pressure (BP), plasma level of glucose, total cholesterol, low density lipoprotein (LDL), very low density lipoprotein (VLDL) and triglycerides (Tgs) were found to be significantly higher whereas high density lipoprotein (HDL) and reduced glutathione were found to be significantly lower among the bank employees as compared with the control subjects. Further, significant alteration in the activity of different enzymes (e.g., glutathione reductase, glutathione S-transferase, glucose 6 phosphate dehydrogenase, catalase and superoxide dismutase) involved in glutathione-mediated antioxidant scavenging systems and increases in lipid peroxidation were also observed in the bank employees. From the study, it appears that the relative risk for cardiovascular disease is increased among bank employees due to the sedentary nature of their jobs.

Adult↗

PubMed2004

Biologic markers of oxidative stress and nephrotoxicity as studied in biomonitoring of adverse effects of occupational exposure to lead and cadmium.

OBJECTIVES: In this work, we studied impregnation levels of workers occupationally exposed to lead (Pb) and cadmium (Cd), usefulness of early urinary markers of nephrotoxicity, and occurrence of oxidative stress as the underlying mechanism involved in Pb- or Cd-induced adverse effects. Thirty-five men were recruited from a nonferrous metal smelter. Pb and Cd in blood (B-Pb, B-Cd) and urine (U-Pb, U-Cd) were measured. Relations between oxidative stress markers (malondialdehyde, superoxide dismutase, glutathione peroxidase, selenium, glutathione reductase, glutathione status, 8-hydroxy-2'-deoxyguanosine) and exposure levels, on the one hand, and early urinary markers (alpha-1-microprotein, beta-2-microglobulin, retinol binding protein, alpha and pi-glutathione S-transferases) and exposure levels, on the other hand, were evaluated. RESULTS: Mean exposure levels were moderate (B-Pb = 395.71 microg Pb/L; U-Pb = 95.19 microg Pb/g creatinine; B-Cd = 5.83 microg Cd/L; U-Cd = 4.67 microg Cd/g creatinine). Changes in malondialdehyde, glutathione status, 8-hydroxy-2'-deoxyguanosine, and alpha-glutathione S-transferases were closely correlated with exposure levels and did not depend on tobacco consumption. We showed that these workers showed moderate Pb and Cd exposure levels. CONCLUSIONS: Taken together, the data suggests the use of alpha-glutathione S-transferases excretion in urine as a hallmark of early changes in the proximal tubular integrity that could later lead to clinical disease if exposure is not reduced.

Adult↗

PubMed1996

Responses of Antioxidative Systems to Drought Stress in Pendunculate Oak and Maritime Pine as Modulated by Elevated CO2.

The aim of the present study was to investigate the effects of an enhanced CO2 concentration alone or in combination with drought stress on antioxidative systems of a deciduous (oak; Quercus robur) and an evergreen (pine; Pinus pinaster) tree species. The seedlings were grown for one season in a greenhouse in tunnels supplied with 350 or 700 [mu]L L-1 CO2. The experiment was repeated in a second year. Antioxidants, protective enzymes, soluble protein, and pigments showed considerable fluctuations in different years. Elevated CO2 caused significant reductions in the activities of superoxide dismutases in both oak and pine. The activities of ascorbate peroxidase and catalase were also reduced in most cases. The activities of dehydroascorbate reductase, monodehydroascorbate radical reductase, glutathione reductase, and guaiacol peroxidase were affected little or not at all by elevated CO2. When the trees were subjected to drought stress by withholding water, the activities of antioxidative enzymes decreased in leaves of pine and oak grown at ambient CO2 and increased in plants grown at elevated CO2 concentrations. The present results suggest that growth in elevated CO2 might reduce oxidative stress to which leaf tissues are normally exposed and enhance metabolic flexibility to encounter increased stress by increases in antioxidative capacity.

Journal Article↗

PubMed1998

Relationship between CO2 Assimilation, Photosynthetic Electron Transport, and Active O2 Metabolism in Leaves of Maize in the Field during Periods of Low Temperature

Measurements of the quantum efficiencies of photosynthetic electron transport through photosystem II (phiPSII) and CO2 assimilation (phiCO2) were made simultaneously on leaves of maize (Zea mays) crops in the United Kingdom during the early growing season, when chilling conditions were experienced. The activities of a range of enzymes involved with scavenging active O2 species and the levels of key antioxidants were also measured. When leaves were exposed to low temperatures during development, the ratio of phiPSII/phiCO2 was elevated, indicating the operation of an alternative sink to CO2 for photosynthetic reducing equivalents. The activities of ascorbate peroxidase, monodehydroascorbate reductase, dehydroascorbate reductase, glutathione reductase, and superoxide dismutase and the levels of ascorbate and alpha-tocopherol were also elevated during chilling periods. This supports the hypothesis that the relative flux of photosynthetic reducing equivalents to O2 via the Mehler reaction is higher when leaves develop under chilling conditions. Lipoxygenase activity and lipid peroxidation were also increased during low temperatures, suggesting that lipoxygenase-mediated peroxidation of membrane lipids contributes to the oxidative damage occurring in chill-stressed leaves.

Journal Article↗

PubMed2004

Amyloid Abeta1-40 preconditions non-apoptotic signals in vivo and protects fetal rat brain from intrauterine ischemic stress.

Abstract The dualistic activities of the amyloid beta (Abeta) peptide as a pro-oxidant and ubiquitous constituent of amyloid deposits in Alzheimer's disease plaques and as an antioxidant of purported physiological function has been suggested but the mechanisms are far from being understood. In this report we measure several oxidative stress parameters and signaling cascades in brains of fetal rats subjected to global ischemia in order to evaluate the putative bifunctional properties of the Abeta(1-40) peptide. Intraperitoneal injection of 6 microg Abeta(1-40) into 18-days-old rat fetuses (approximately 3 g body weight) resulted after 24 h in the appearance of the peptide in various fetal organs including brain where it enhanced the levels of glutathione (GSH), glutathione reductase, glutathione peroxidase, and stimulated the levels of pro-survival signaling activities such as Akt serine/threonine kinase, extracellular signal-regulated kinase (ERK) and protein kinase C enzymes. Moreover, pretreatment with Abeta(1-40) reversed the consequences of a transient hypovolemic/hypotensive oxidative stress by restoring GSH levels via its recycling enzymes and by lowering the production of lipid peroxides presumably by activating the aforementioned pro-survival signaling cascades. It also caused a reduction in the number of DAPI-enhanced reactive cells and a decrease in p38 kinase phosphorylation and caspase-9 and -3 activity. These data suggest that pre-exposure to Abeta(1-40) stimulates fetal tolerance to ischemia via regulation of GSH metabolism and as such may be considered as neuroprotective.

Amyloid beta-Peptides↗

PubMed2005

Melatonin reduces oxidative stress and increases gene expression in the cerebral cortex and cerebellum of aluminum-exposed rats.

The pro-oxidant activity of aluminum (Al), the protective role of exogenous melatonin, as well as the mRNA levels of some antioxidant enzymes, were determined in cortex and cerebellum of rats following exposure to Al and/or melatonin. Two groups of male rats received intraperitoneal injections of Al lactate or melatonin at doses of 7 mg Al/kg/day and 10 mg/kg/day, respectively, for 11 wk. A third group of animals received concurrently Al lactate (7 mg Al/kg/day) plus melatonin (10 mg/kg/day) during the same period. A fourth group of rats was used as control. At the end of the treatment, the cerebral cortex and cerebellum were removed and processed to examine the following oxidative stress markers: glutathione transferase (GST), reduced glutathione (GSH), oxidized glutathione (GSSG), superoxide dismutase (SOD), glutathione reductase, glutathione peroxidase (GPx), catalase (CAT), thiobarbituric acid reactive substances (TBARS), as well as protein content. Moreover, gene expression of Cu-ZnSOD, MnSOD, GPx and CAT was evaluated by real-time RT-PCR. On the other hand, Al, Fe, Mn, Cu and Zn concentrations were determined in cortex and cerebellum of rats. Oxidative stress was promoted in both neural regions following Al administration, resulting from the pro-oxidant activity related with an increase in tissue Al concentrations. In contrast, melatonin exerted an antioxidant action which was related with an increase in the mRNA levels of the antioxidant enzymes evaluated. The results of the present investigation emphasize the potential use of melatonin as a supplement in the therapy of neurological disorders in which oxidative stress is involved.

Aluminum↗

PubMed1989

Isolation of an atypically small lipoamide dehydrogenase involved in the glycine decarboxylase complex from Eubacterium acidaminophilum.

The lipoamide dehydrogenase of the glycine decarboxylase complex was purified to homogeneity (8 U/mg) from cells of the anaerobe Eubacterium acidaminophilum that were grown on glycine. In cell extracts four radioactive protein fractions labeled with D-[2-14C]riboflavin could be detected after gel filtration, one of which coeluted with lipoamide dehydrogenase activity. The molecular mass of the native enzyme could be determined by several methods to be 68 kilodaltons, and an enzyme with a molecular mass of 34.5 kilodaltons was obtained by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Immunoblot analysis of cell extracts separated by sodium dodecyl sulfate-polyacrylamide or linear polyacrylamide gel electrophoresis resulted in a single fluorescent band. NADPH instead of NADH was the preferred electron donor of this lipoamide dehydrogenase. This was also indicated by Michaelis constants of 0.085 mM for NADPH and 1.1 mM for NADH at constant lipoamide and enzyme concentrations. The enzyme exhibited no thioredoxin reductase, glutathione reductase, or mercuric reductase activity. Immunological cross-reactions were obtained with cell extracts of Clostridium cylindrosporum, Clostridium sporogenes, Clostridium sticklandii, and bacterium W6, but not with extracts of other glycine- or purine-utilizing anaerobic or aerobic bacteria, for which the lipoamide dehydrogenase has already been characterized.

Amino Acid Oxidoreductases↗

PubMed2004

Microarray analyses identify molecular biomarkers of Atlantic salmon macrophage and hematopoietic kidney response to Piscirickettsia salmonis infection.

Piscirickettsia salmonis is the intracellular bacterium that causes salmonid rickettsial septicemia, an infectious disease that kills millions of farmed fish each year. The mechanisms used by P. salmonis to survive and replicate within host cells are not known. Piscirickettsiosis causes severe necrosis of hematopoietic kidney. Microarray-based experiments with QPCR validation were used to identify Atlantic salmon macrophage and hematopoietic kidney genes differentially transcribed in response to P. salmonis infection. Infections were confirmed by microscopy and RT-PCR with pathogen-specific primers. In infected salmon macrophages, 71 different transcripts were upregulated and 31 different transcripts were downregulated. In infected hematopoietic kidney, 30 different transcripts were upregulated and 39 different transcripts were downregulated. Ten antioxidant genes, including glutathione S-transferase, glutathione reductase, glutathione peroxidase, and cytochrome b558 alpha- and beta-subunits, were upregulated in infected macrophages but not in infected hematopoietic kidney. Changes in redox status of infected macrophages may allow these cells to tolerate P. salmonis infection, raising the possibility that treatment with antioxidants may reduce hematopoietic tissue damage caused by this rickettsial infection. The downregulation of transcripts involved in adaptive immune responses (e.g., T cell receptor alpha-chain and C-C chemokine receptor 7) in infected hematopoietic kidney but not in infected macrophages may contribute to infection-induced kidney tissue damage. Molecular biomarkers of P. salmonis infection, characterized by immune-relevant functional annotations and high fold differences in expression between infected and noninfected samples, may aid in the development of anti-piscirickettsial vaccines and therapeutics.

Animals↗

PubMed1998

Targeted lung expression of interleukin-11 enhances murine tolerance of 100% oxygen and diminishes hyperoxia-induced DNA fragmentation.

Acute lung injury is a frequent and treatment-limiting consequence of therapy with hyperoxic gas mixtures. To determine if IL-11 is protective in oxygen toxicity, we compared the effects of 100% O2 on transgenic mice that overexpress IL-11 in the lung and transgene (-) controls. IL-11 markedly enhanced survival in 100% O2 with 100% of transgene (-) animals dying within 72-96 h and > 90% of transgene (+) animals surviving for more than 10 d. This protection was associated with markedly diminished alveolar-capillary protein leak, endothelial and epithelial membrane injury, lipid peroxidation, and pulmonary neutrophil recruitment. Significant differences in copper zinc superoxide dismutase and catalase activities were not noted and the levels of total, reduced and oxidized glutathione were similar in transgene (+) and (-) animals. Glutathione reductase, glutathione peroxidase, and manganese superoxide dismutase activities were slightly higher in transgene (+) as versus (-) mice after 100% O2 exposure, and IL-11 diminished hyperoxia-induced expression of IL-1 and TNF. Hyperoxia also caused cell death with DNA fragmentation in the lungs of transgene (-) animals and IL-11 markedly diminished this cell death response. These studies demonstrate that IL-11 markedly diminishes hyperoxic lung injury. They also demonstrate this protection is associated with small changes in lung antioxidants, diminished hyperoxia-induced IL-1 and TNF production, and markedly suppressed hyperoxia-induced DNA fragmentation.

Animals↗

PubMed2005

Neuroprotective effects of Withania somnifera on 6-hydroxydopamine induced Parkinsonism in rats.

6-Hydroxydopamine (6-OHDA) is one of the most widely used rat models for Parkinson's disease. There is ample evidence in the literature that 6-OHDA elicits its toxic manifestations through oxidant stress. In the present study, we evaluated the anti-parkinsonian effects of Withania somnifera extract, which has been reported to have potent anti-oxidant, anti-peroxidative and free radical quenching properties in various diseased conditions. Rats were pretreated with 100, 200 and 300 mg/kg b.w. of the W. somnifera extract orally for 3 weeks. On day 21, 2 microL of 6-OHDA (10 microg in 0.1% in ascorbic acid-saline) was infused into the right striatum while sham operated group received 2 microL of the vehicle. Three weeks after 6-OHDA injections, rats were tested for neurobehavioral activity and were killed 5 weeks after lesioning for the estimation of lipidperoxidation, reduced glutathione content, activities of glutathione-S-transferase, glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase, catecholamine content, dopaminergic D2 receptor binding and tyrosine hydroxylase expression. W. somnifera extract was found to reverse all the parameters significantly in a dose-dependent manner. Thus, the study demonstrates that the extract of W. somnifera may be helpful in protecting the neuronal injury in Parkinson's disease.

Animals↗

PubMed2006

Use of the land snail Helix aspersa as sentinel organism for monitoring ecotoxicologic effects of urban pollution: an integrated approach.

Atmospheric pollution from vehicular traffic is a matter of growing interest, often leading to temporary restrictions in urban areas. Although guidelines indicate limits for several parameters, the real toxicologic impacts remain largely unexplored in field conditions. In this study our aim was to validate an ecotoxicologic approach to evaluate both bioaccumulation and toxicologic effects caused by airborne pollutants. Specimens of the land snail Helix aspersa were caged in five sites in the urban area of Ancona, Italy. After 4 weeks, trace metals (cadmium, chromium, copper, iron, manganese, nickel, lead, and zinc) and polycyclic aromatic hydrocarbons (PAHs) were measured and these data integrated with the analyses of molecular and biochemical responses. Such biomarkers reflected the induction of detoxification pathways or the onset of cellular toxicity caused by pollutants. Biomarkers that correlated with contaminant accumulation included levels of metallothioneins, activity of biotransformation enzymes (ethoxyresorufin O-deethylase, ethoxycoumarin O-deethylase), and peroxisomal proliferation. More general responses were investigated as oxidative stress variations, including efficiency of antioxidant defenses (catalase, glutathione reductase, glutathione S-transferases, glutathione peroxidases, and total glutathione) and total oxyradical scavenging capacity toward peroxyl and hydroxyl radicals, onset of cellular damages (i.e., lysosomal destabilization), and loss of DNA integrity. Results revealed a marked accumulation of metals and PAHs in digestive tissues of organisms maintained in more traffic-congested sites. The contemporary appearance of several alterations confirmed the cellular reactivity of these chemicals with toxicologic effects of potential concern for human health. The overall results of this exploratory study suggest the utility of H. aspersa as a sentinel organism for biomonitoring the biologic impact of atmospheric pollution in urban areas. Key words: atmospheric pollutants, bioindicators, biomarkers, DNA integrity, lysosomes, metallothioneins, oxidative stress, peroxisomes, polycyclic aromatic hydrocarbons, trace metals.

Air Pollutants↗

PubMed1988

The biochemistry of endogenous organosulphur compounds.

The role and metabolism of methionine and cysteine in mammals are described. An outline of the history of glutathione, of its function in maintaining the thiol status of the cell and of its protective action against oxidative stress, is given. The importance of glutathione reductase, glutathione peroxidases, glutathione-S-transferases in endogenous metabolism and of gamma-glutamyltranspeptidase is described. The relationship between cysteine and glutathione is considered together with the inter-organ translocation of glutathione and its metabolism.

Animals↗

PubMed2003

The secondary alcohol and aglycone metabolites of doxorubicin alter metabolism of human erythrocytes.

Anthracyclines, a class of antitumor drugs widely used for the treatment of solid and hematological malignancies, cause a cumulative dose-dependent cardiac toxicity whose biochemical basis is unclear. Recent studies of the role of the metabolites of anthracyclines, i.e., the alcohol metabolite doxorubicinol and aglycone metabolites, have suggested new hypotheses about the mechanisms of anthracycline cardiotoxicity. In the present study, human red blood cells were used as a cell model. Exposure (1 h at 37 C) of intact human red blood cells to doxorubicinol (40 M) and to aglycone derivatives of doxorubicin (40 M) induced, compared with untreated red cells: i) a ~2-fold stimulation of the pentose phosphate pathway (PPP) and ii) a marked inhibition of the red cell antioxidant enzymes, glutathione peroxidase (~20%) and superoxide dismutase (~60%). In contrast to doxorubicin-derived metabolites, doxorubicin itself induced a slighter PPP stimulation (~35%) and this metabolic event was not associated with any alteration in glutathione reductase, glutathione peroxidase, catalase or superoxide dismutase activity. Furthermore, the interaction of hemoglobin with doxorubicin and its metabolites induced a significant increase (~22%) in oxygen affinity compared with hemoglobin incubated without drugs. On the basis of the results obtained in the present study, a new hypothesis, involving doxorubicinol and aglycone metabolites, has been proposed to clarify the mechanisms responsible for the doxorubicin-induced red blood cell toxicity.

Antibiotics, Antineoplastic↗

PubMed2003

Biomarker responses and chemical analyses in fish indicate leakage of polycyclic aromatic hydrocarbons and other compounds from car tire rubber.

Rubber tire material contains toxic compounds including oils rich in polycyclic aromatic hydrocarbons (PAH), so-called highly aromatic (HA) oils, as well as other reactive additives used as antioxidants, antiozonants, and vulcanization accelerators. The toxicity of rubber tire leachates to aquatic organisms has been demonstrated before. However, previous studies have focused on lethal rather than sublethal effects. We kept rainbow trout (Oncorhynchus mykiss) in tanks with two types of tires: a tire containing HA oils in the tread or a tire free of HA oils in the tread. After 1 d of exposure, an induction of cytochrome P4501A1 (CYP1A1) was evident in both exposed groups, measured as elevated ethoxyresorufin-O-deethylase (EROD) activity and increased CYP1A1 mRNA levels. After two weeks of exposure, EROD activity and CYP1A1 mRNA were still high in fish exposed to leachate from HA oil-containing tire, whereas the effect was somewhat lower in fish exposed to leachate from HA oil-free tread tire. Compounds in the tire leachates also affected antioxidant parameters. Total glutathione concentration in liver as well as hepatic glutathione reductase, glutathione S-transferase, and glucose-6-phosphate dehydrogenase activities were markedly elevated after two weeks of exposure in both groups. The responses were greater in the group exposed to leachate from HA oil-free tread tire. Vitellogenin measurements did not indicate leakage of estrogenic compounds from the tires. Chemical analyses of bile from exposed fish revealed the presence of hydroxylated PAH as well as aromatic nitrogen compounds indicating uptake of these compounds by the fish.

Animals↗

PubMed2005

Interactions between metabolism of trace metals and xenobiotic agonists of the aryl hydrocarbon receptor in the antarctic fish Trematomus bernacchii: environmental perspectives.

Although Antarctica is a pristine environment, organisms are challenged with contaminants either released locally or transported from industrialized regions through atmospheric circulation and marine food webs. Organisms from Terra Nova Bay also are exposed to a natural enrichment of cadmium, but to our knowledge, whether such environmental conditions influence biological responses to anthropogenic pollutants has never been considered. In the present study, the Antarctic rock cod (Trematomus bernacchii) was exposed to model chemicals, including polycyclic aromatic hydrocarbons (benzo[a]pyrene), persistent organic pollutants (2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD]), cadmium, and a combination of cadmium and TCDD. Analyzed parameters included chemical bioaccumulation, activity, and levels of biotransformation enzymes (cytochrome P4501A); metallothioneins and the efficiency of the antioxidant system measured as individual defenses (catalase, glutathione, glutathione reductase, glutathione S-transferases, and glutathione peroxidases); and total scavenging capacity toward peroxyl and hydroxyl radicals. Reciprocal interactions between metabolism of inorganic and organic pollutants were demonstrated. Dioxin enhanced the accumulation of cadmium, probably stored within proliferating endoplasmic reticulum, and cadmium suppressed the inducibility of cytochrome P4501A, allowing us to hypothesize a posttranscriptional mechanism as the depletion of heme group availability. Clear evidence of oxidative perturbation was provided by the inhibition of antioxidants and enhanced sensitivity to oxyradical toxicity in fish exposed to organic chemicals. Exposure to cadmium revealed counteracting responses of glutathione metabolism; however, these responses did not prevent a certain loss of antioxidant capacity toward peroxyl radicals. The pattern of antioxidant responses exhibited by fish coexposed to cadmium and TCDD was more similar to that observed for cadmium than to that observed for TCDD. The overall results suggest that elevated natural levels of cadmium in Antarctic organisms from Terra Nova Bay can limit biotransformation capability of polycyclic (halogenated) hydrocarbons, thus influencing the bioaccumulation and biological effects of these chemicals in key sentinel species.

Animals↗

PubMed2006

Toxic effects and oxidative stress in higher plants exposed to polycyclic aromatic hydrocarbons and their N-heterocyclic derivatives.

N-heterocyclic derivatives of polycyclic aromatic hydrocarbons (NPAHs) are widespread concomitantly with their parent analogues and have been detected in air, water, sediments, and soil. Although they were shown to be highly toxic to some organisms, our understanding of their occurrence, environmental fate, biological metabolism, and effects is limited. This study evaluated toxic effects of three homocyclic aromatic hydrocarbons (PAHs-phenanthrene, anthracene, fluorene) and their seven N-heterocyclic derivates on higher terrestrial plants Sinapis alba, Triticum aestivum, and Phaseolus vulgaris. Germinability, morphological endpoints, parameters of detoxification, and antioxidant components of plant metabolism as well as lipid peroxidation were studied in acute phytotoxicity tests. Phytotoxicity of NPAHs was generally more pronounced than the effects of parent PAHs, and it significantly differed with respect to the structure of individual NPAHs. Sinapis alba and T. aestivum were more sensitive plant species than P. vulgaris. Chemicals with the strongest inhibition effect on germination and growth of plants were phenanthridine, acridine, benzo[h]quinoline, and 1,10- and 1,7-phenanthroline. All tested chemicals significantly induced activities of detoxification and antioxidant enzymes (glutathione reductase, glutathione peroxidase, and glutathione-S-transferase) at nanomolar to low micromolar concentrations. Levels of reduced glutathione were induced by all tested chemicals except 1,10- and 4,7-phenanthroline. Furthermore, fluorene, carbazole, acridine, phenanthrene, phenanthridine, benzo[h]quinoline, and 1,7-phenanthroline significantly increased lipid peroxidation. The results of our study newly demonstrate significant toxicity of NPAHs to plants and demonstrate suitability of multiple biomarker assessment to characterize mechanisms of oxidative stress and to serve as an early warning of phytotoxicity in vivo.

Biomass↗

PubMed1980

The effects of adriamycin (doxorubicin HCl) on human red blood cells.

We have studied the effects of adriamycin (doxorubicin HCl) on human red blood cells. The peroxidizing effect of adriamycin on the thiols of red cell constituents resulted in decreased glutathione stability, and oxidation of hemoglobin and membrane protein components 1, 2, and 3, forming large molecular weight complexes. Membrane lipids were also peroxidized. Adriamycin itself did not inhibit the enzymes of the reductions system (glucose-6-phosphate dehydrogenase, 6-phosphogluconic dehydrogenase, glutathione reductase, glutathione peroxidase, catalase, superoxide dismutase) of the red cells. Because adriamycin has the potential of inhibiting ATPase, including both Na-K-dependent ATPase and ouabain insensitive ATPase, at concentrations not inhibitory to other enzymes, the net sodium content increased, and potassium content decreased after incubation of red cells with adriamycin at high concentrations. The experimental results described with adriamycin may serve as a model for the possible mechanism of cardiotoxicity observed in its clinical use, and also explain the potential hemolyzing effect on red cells. There was greater oxidizing effect on glucose-6-phosphate dehydrogenase (G-6-PD) deficient than on normal erythrocytes. It is suggested that adriamycin be used with caution in individuals with G-6-PD deficient red cells.

Adenosine Triphosphatases↗