Ex vivo comparison of CBCT and digital periapical radiographs for the quantitative assessment of periodontal defects.

OBJECTIVES: Accurate imaging is essential for effective treatment planning in periodontology. The aim of this ex vivo study was to investigate the accuracy of cone beam computed tomography (CBCT) and digital periapical radiographs (PA) in imaging periodontal defects. Hypotheses are: 1. That CBCT is a more accurate method than PA concerning vertical measurements of periodontal bone defects2. That CBCT itself is an accurate method to describe vertical periodontal bone loss MATERIAL AND METHODS: In this study, 117 periodontal defects from 10 human cadavers were investigated radiographically by CBCT and PA by one calibrated observer. Afterwards the vertical bone loss was measured with a periodontal probe by the same calibrated observer. Differences between radiographic and clinical measurements were calculated and analyzed. Bland-Altmann plots including 95% limits of agreement were calculated. RESULTS: The 95% limits of agreement ranged from 3.29 to -3.27 mm between clinical measurements and measurements in PAs, and from 2.13 to -1.97 mm in CBCTs. The mean difference between clinical and radiographic measurements was 0.0009 mm for PA and 0.0835 mm for CBCT. CONCLUSIONS: When comparing the clinical measurements, CBCT had a higher agreement and less deviations than PAs, and CBCT seems to be an accurate method to describe vertical periodontal bone loss. CLINICAL RELEVANCE: Accurate description of defects is helpful for accurate treatment planning.

Detection and putative effect of GATA4 gene variants in patients with congenital cardiac septal defects.

The zinc finger transcription factor GATA4, located on chromosome 8p23.1-p22, has been implicated as a critical regulator of cardiac development during embryogenesis. Mutations of GATA4 appear to be responsible for some cardiac septal defects. The aim of this work was to screen for mutations in the GATA4 gene in sample of Egyptian patients affected by isolated and non-isolated cardiac septal defects. We examined 20 patients with atrial septal defect (ASD), ventricle septal defect (VSD), atrioventricular septal defects (AVSD) and A-V canal disturbance defect and compared with examined 10 unaffected individuals as normal control. The patients were referred from Congenital Heart Disease Clinic of the Clinical Genetics department at the National Research Centre. All patients were subjected to clinical evaluation, echocardiography and karyotyping. Genomic DNA was extracted from all cases and subjected to PCR followed by direct sequencing. The predicted effect of variants was done by a variety of proper prediction tools. We detected six variants in GATA4 gene, two of them are novel variants. Predicted functional analysis of the relevant variants was performed by In silico analysis. Further confirmatory studies on familial segregation and in vitro / in vivo functional analysis are recommended to support our results.

Genetic diversity and antibiotic resistance in Shigella dysenteriae and Shigella boydii strains isolated from children aged <5 years in Egypt.

Diversity within Shigella dysenteriae (n=40) and Shigella boydii (n=30) isolates from children living in Egypt aged <5 years was investigated. Shigella-associated diarrhoea occurred mainly in summer months and in children aged <3 years, it commonly presented with vomiting and fever. Serotypes 7 (30%), 2 (28%), and 3 (23%) accounted for most of S. dysenteriae isolates; 50% of S. boydii isolates were serotype 2. S. dysenteriae and S. boydii isolates were often resistant to ampicillin, chloramphenicol and tetracycline (42%, 17%, respectively), although resistance varied among serotypes. Pulsed-field gel electrophoresis separated the isolates into distinct clusters correlating with species and serotype. Genetic differences in trimethoprim/sulfamethoxazole and ß-lactam-encoding resistance genes were also evident. S. dysenteriae and S. boydii are genetically diverse pathogens in Egypt; the high level of multidrug resistance associated with both pathogens and resistance to the most available inexpensive antibiotics underlines the importance of continuing surveillance.

A unique, inexpensive, and abundantly available adsorbent: composite of synthesized silver nanoparticles (AgNPs) and banana leaves powder (BLP).

The purpose of this study is to investigate the development of a new and inexpensive adsorbent by immobilization synthesized silver nanoparticles (AgNPs) onto banana leaves powder (BLP), and the prepared composite (BLP)/(AgNPs) was used as an adsorbent for Zn(II), Pb(II), and Fe(III) ion removal from aqueous solutions under the influence of various reaction conditions. (BLP)/(AgNPs) demonstrated remarkable sensitivity toward Zn (II), Pb (II), and Fe (III) ions; metal ions eliminations increased with increasing contact time, agitation speed, adsorbent dose, and temperature, yielding adequate selectivity and ideal removal efficiency of 79%, 88%, and 91% for Zn (II), Pb (II), and Fe (III) ions, respectively, at pH = 5 for Zn(II) and pH = 6 for Pb(II), and Fe(III). The equilibrium contact time for elimination of Zn (II), Pb (II), and Fe (III) ions was reaches at 40 min. Langmuir, Freundlich, and Temkin equations were used to test the obtained experimental data. Langmuir isotherm model was found to be more accurate in representing the data of Zn(II), Pb(II), and Fe(III) ions adsorption onto (BLP)/(AgNPs), with a regression coefficient (R2 = 0.999) and maximum adsorption capacities of 190, 244, and 228 mg/g for Zn(II), Pb(II), and Fe(III) ions, respectively. The thermodynamic parameters proved that adsorption of metal ions is spontaneous, feasible, and endothermic, whereas Kinetic studies revealed that the process was best described by a pseudo second order kinetics.

Expression of Hsp70, Igf1, and Three Oxidative Stress Biomarkers in Response to Handling and Salt Treatment at Different Water Temperatures in Yellow Perch, Perca flavescens.

Stress is a major factor that causes diseases and mortality in the aquaculture industry. The goal was to analyze the expression of stress-related biomarkers in response to different stressors in yellow perch, which is an important aquaculture candidate in North America and highly sensitive to handling in captivity. Three fish groups were established, each having four replicates, and subjected to water temperatures of 14, 20, and 26°C and acute handling stress was performed followed by a salt treatment for 144h at a salinity of 5 ppt. Serum and hepatic mRNA levels of heat shock protein (hsp70), insulin-like growth factor 1 (Igf1), glutathione peroxidase (Gpx), superoxide dismutase 1 (Sod1), and glutathione reductase (Gsr) were quantified at seven times interval over 144 h using ELISA and RT-qPCR. Handling stress caused a significant down-regulation in Hsp70, Gpx, Sod1, and Gsr at a water temperature of 20°C compared to 14 and 26°C. Igf1 was significantly upregulated at 20°C and down-regulated at 14 and 26°C. Salt treatment had a transient reverse effect on the targeted biomarkers in all groups at 72 h, then caused an upregulation after 144 h, compared to the control groups. The data showed a negative strong regulatory linear relationship between igf1 with hsp70 and anti-oxidative gene expressions. These findings could provide valuable new insights into the stress responses that affect fish health and could be used to monitor the stress.

Pulmonary microsomes contain a Ca(2+)-transport system sensitive to oxidative stress.

A variety of events, including inhalation of atmospheric chemicals, trauma, and ischemia-reperfusion, may cause generation of reactive oxygen species in the lung and result in airways constriction. The specific metabolic mechanisms that translate oxygen radical production into airways constriction are yet to be identified. In the lung, calcium homeostasis is central to release of bronchoactive and vasoactive chemical mediators and to regulation of smooth muscle cell contractility, i.e., airway constriction. In the present work, we characterized Ca(2+)-transport in the microsomal fraction of mouse lungs, and determined how reactive oxygen species, generated by Fe2+/ascorbate and H2O2/hemoglobin, affected Ca2+ transport. The microsomal fraction of pulmonary tissue accumulated 90 +/- 5 nmol Ca2+/mg protein by an ATP-dependent process in the presence of 15 mM oxalate, and 16 +/- 2 nmol Ca2+ in its absence. In the presence of oxalate, the rate of Ca2+ uptake was 50 +/- 5 nmol Ca2+/min per mg protein at pCa 5.9 (37 degrees C). The Ca(2+)-ATPase activity was 50-60 nmol Pi/min per mg protein (pCa 5.9, 37 degrees C) in the presence of alamethicin. Inhibitors of mitochondrial H(+)-ATPase had no effect on the Ca2+ transport. Half-maximal activation of Ca2+ transport was produced by 0.4-0.5 microM Ca2+. Endoplasmic reticulum Ca(2+)-pump (SERC-ATPase) was found to be predominantly responsible for the Ca(2+)-accumulating capacity of the pulmonary microsomes. Incubation of the microsomes in the presence of either Fe2+/ascorbate or H2O2/hemoglobin resulted in a time-dependent accumulation of peroxidation products (TBARS) and in inhibition of the Ca2+ transport. The inhibitory effect of Fe2+/ascorbate on Ca2+ transport strictly correlated with the inhibition of the Ca(2+)-ATPase activity. These results are the first to indicate a highly active microsomal Ca2+ transport system in murine lungs which is sensitive to endogenous oxidation products. The importance of this system to pulmonary disorders exacerbated by oxidative chemicals remains to be studied.

Effects of food restriction and hyperoxia on rat survival and lung polyamine metabolism.

We fed Sprague-Dawley rats either freely or by restricting them to 20% of their usual diet for 21 days. In one experiment, we refed half of the food-restricted rats for 12 h, then exposed the three groups to air or 85% O2 for 5 days. The mortalities in 85% O2 were 100, 33, and 0% for the food-restricted, restricted-refed, and freely fed groups, respectively. In air lung polyamine contents and glucose 6-phosphate dehydrogenase and NADP-dependent isocitrate dehydrogenase activities were significantly lower with food restriction. After hyperoxia, lung polyamine and protein contents and enzyme activities were increased in the two surviving groups, but spermine and DNA contents of refed rats did not increase. In a second experiment, we exposed rats to 60% O2 and found that DNA synthesis of food-restricted rats was lower than the freely fed rats in air and remained low after hyperoxia. We conclude that food restriction increases the mortality from 85% O2 and is associated with lower DNA synthesis and polyamine content. We speculate that food-restricted animals may accumulate greater lung injury partly because of a compromised repair process.

Toxicity of nitrogen dioxide: an introduction.

Many questions, needed to advance our understanding of the mechanism of injury from high-level NO2, remain unanswered to date. This is partly due to the limited interest in the toxicity of high-level exposures, and partly due to the public pressure and interest to study the effects of low- (environmental) levels. However, the effects of exposure to high-level NO2 are of great interest to the military since high levels of NO2 may be found in combat situations. It is also important to the civilian section in occupational settings where accidents may occur as in silo filler accidents. To fill this gap in knowledge, the Department of Respiratory Research, Division of Medicine at Walter Reed Army Institute of Research took the initiative and convened a panel of experts in a symposium to discuss in depth the effects of exposure to high-level nitrogen dioxide. The symposium goals were to address the issues beginning from the chemistry of NO2 molecule, to the dosimetry of its uptake (isolated lung), to the biological effects of exposure in vivo in small animals (rats), large animals (sheep), and finally in the most relevant species, humans.

Toxicology of blast overpressure.

Blast overpressure (BOP) or high energy impulse noise, is the sharp instantaneous rise in ambient atmospheric pressure resulting from explosive detonation or firing of weapons. Blasts that were once confined to military and to a lesser extent, occupational settings, are becoming more universal as the civilian population is now increasingly at risk of exposure to BOP from terrorist bombings that are occurring worldwide with greater frequency. Exposure to incident BOP waves can cause auditory and non-auditory damage. The primary targets for BOP damage are the hollow organs, ear, lung and gastrointestinal tract. In addition, solid organs such as heart, spleen and brain can also be injured upon exposure. However, the lung is more sensitive to damage and its injury can lead to death. The pathophysiological responses, and mortality have been extensively studied, but little attention, was given to the biochemical manifestations, and molecular mechanism(s) of injury. The injury from BOP has been, generally, attributed to its external physical impact on the body causing internal mechanical damage. However, a new hypothesis has been proposed based on experiments conducted in the Department of Respiratory Research, Walter Reed Army Institute of Research, and later in the Department of Occupational Health, University of Pittsburgh. This hypothesis suggests that subtle biochemical changes namely, free radical-mediated oxidative stress occur and contribute to BOP-induced injury. Understanding the etiology of these changes may shed new light on the molecular mechanism(s) of injury, and can potentially offer new strategies for treatment. In this symposium. BOP research involving auditory, non-auditory, physiological, pathological, behavioral, and biochemical manifestations as well as predictive modeling and current treatment modalities of BOP-induced injury are discussed.

Diet restriction modulates lung response and survivability of rats exposed to ozone.

Ozone (O(3)) is a powerful oxidant component of photochemical smog polluting the air of urban cities. Exposure to low-level O(3) causes lung injury and increased morbidity of the sensitive segment of population, and exposure to high levels can be lethal to experimental animals. Injury from O(3) exposure is generally associated with free radical formation and oxidative stress. Because diet restriction is proposed to enhance antioxidant status, we examined whether it would influence the response to inhaled O(3). Twenty-four Sprague-Dawley rats, 1 month old, weighing 150 g, were divided into two dietary regimens (12 rats/regimen); one was freely-fed (FF), and the second was diet-restricted (DR) to 20% the average daily intake of the FF. After 60 days of dietary conditioning, the body weight of DR rats was reduced to 50% that of FF rats. Then, in one experiment, two groups (six rats/group), one FF and the other DR, were exposed to 0.8+/-0.1 p.p.m. (1570+/-196 microg/m(3)) O(3), continuously for 3 days. Another two similar groups of rats were exposed to filtered room air and served as matched controls. After exposure, all rats were euthanized and the lungs analyzed for biochemical markers of oxidative stress. In a second experiment, 24 rats were divided into two groups (12 rats/group), one FF and the other DR, then exposed to high-level O(3) for 8 h (4 p.p.m., 7848+/-981 microg/m(3)) and the mortality noted during exposure and for 16 h post-exposure. Following low-level O(3), inhalation, greater alterations were observed in FF rats compared with DR rats. With high-level O(3) exposure, DR rats exhibited a much greater survivability compared with FF rats (90% versus 8%, respectively). These observations suggest that diet restriction leading to significant reduction of body weight is beneficial, and may play a role in the resistance to the adverse effects of O(3).

Visual system degeneration induced by blast overpressure.

The effect of blast overpressure on visual system pathology was studied in 14 male Sprague-Dawley rats weighing 360-432 g. Blast overpressure was simulated using a compressed-air driven shock tube, with the aim of studying a range of overpressures causing sublethal injury. Neither control (unexposed) rats nor rats exposed to 83 kiloPascals (kPa) overpressure showed evidence of visual system pathology. Neurological injury to brain visual pathways was observed in male rats surviving blast overpressure exposures of 104-110 kPa and 129-173 kPa. Optic nerve fiber degeneration was ipsilateral to the blast pressure wave. The optic chiasm contained small numbers of degenerated fibers. Optic tract fiber degeneration was present bilaterally, but was predominantly ipsilateral. Optic tract fiber degeneration was followed to nuclear groups at the level of the midbrain, midbrain-diencephalic junction, and the thalamus where degenerated fibers arborized among the neurons of: (i) the superior colliculus, (ii) pretectal region, and (iii) the lateral geniculate body. The superior colliculus contained fiber degeneration localized principally to two superficial layers (i) the stratum opticum (layer III) and (ii) stratum cinereum (layer II). The pretectal area contained degenerated fibers which were widespread in (i) the nucleus of the optic tract, (ii) olivary pretectal nucleus, (iii) anterior pretectal nucleus, and (iv) the posterior pretectal nucleus. Degenerated fibers in the lateral geniculate body were not universally distributed. They appeared to arborize among neurons of the dorsal and ventral nuclei: the ventral lateral geniculate nucleus (parvocellular and magnocellular parts); and the dorsal lateral geniculate nucleus. The axonopathy observed in the central visual pathways and nuclei of the rat brain are consistent with the presence of blast overpressure induced injury to the retina. The orbital cavities of the human skull contain frontally-directed eyeballs for binocular vision. Humans looking directly into an oncoming blast wave place both eyes at risk. With bilateral visual system injury, neurological deficits may include loss or impairments of ocular movements, and of the pupillary and accommodation reflexes, retinal hemorrhages, scotomas, and general blindness. These findings suggest that the retina should be investigated for the presence of traumatic or ischemic cellular injury, hemorrhages, scotomas, and retinal detachment.

Exposure to sublethal blast overpressure reduces the food intake and exercise performance of rats.

Exposure to blast overpressure can typically inflict generalized damage on major organ systems, especially gas-containing organs such as the lungs and the gastrointestinal tract. The purpose of the present study was to use rat's food intake and exercise wheel running as behavioral correlates of the perhaps more subtle damage to these organ systems induced by sublethal blast overpressure. Toward this end, all rats were exposed to a 12-h light/dark cycle and food was available only in the dark period. Prior to exposure, rats in the (E)xercise group were required to execute five rotations of an activity wheel for a food pellet; wheel turns that occurred at times other than when a rat was feeding were recorded separately and labeled exercise running. In the (S)edentary and (A)nesthesia groups, wheel running was not possible and rats were required to execute five leverpresses for a single pellet. A compressed air-driven shock tube was used to expose rats to a supra-atmospheric wave of air pressure. The tube was separated into two sections by a polyester membrane, the thickness of which determined peak and duration of overpressure. All rats were anesthetized with 50 mg/kg of phenobarbital. After reaching a deep plane of anesthesia, they were individually tied in a stockinet across one end of the shock tube. In preliminary tests, the membrane thickness was 1000 (A)ngstroms and rats in Group L(ethality) were exposed to a 129 kPa (peak amplitude) wave of overpressure. Three of six rats survived exposure to this peak pressure; pathology was evident in the lungs and gastrointestinal tract of all non-survivors. Rats in Groups E and S were tested with a 500 A membrane, which resulted in an 83 kPa peak amplitude. All rats survived exposure to this lower peak pressure. On the day of exposure to blast, the relative reduction of intake during the first 3 h of the dark period was significantly greater for Group E than for Groups S and A; the intake of Groups E and S remained reduced for four additional recovery days. Bodyweight was not significantly affected. Exercise wheel running also was reduced significantly on the day of exposure and during subsequent recovery days. These preliminary findings suggest that exposure to sublethal blast overpressure can reduce food consumption and exercise performance, perhaps as a consequence of damage to the gastrointestinal tract and lungs.

A proposed biochemical mechanism involving hemoglobin for blast overpressure-induced injury.

Blast overpressure (BOP) is the abrupt, rapid, rise in atmospheric pressure resulting from explosive detonation, firing of large-caliber weapons, and accidental occupational explosions. Exposure to incident BOP waves causes internal injuries, mostly to the hollow organs, particularly the ears, lungs and gastrointestinal tract. BOP-induced injury used to be considered of military concern because it occurred mostly in military environments during military actions or training, and to a lesser extent during civilian occupational accidents. However, in recent years with the proliferation of indiscriminate terrorist bombings worldwide involving civilians, blast injury has become a societal concern, and the need to understand the biochemical and molecular mechanism(s) of injury, and to find new and effective methods for treatment gained importance. In general, past BOP research has focused on the physiological and pathological manifestations of incapacitation, thresholds of safety, and on predictive modeling. However, we have been studying the molecular mechanism of BOP-induced injury, and recently began to have an insight into that mechanism, and recognize the role of hemoglobin released during hemorrhage in catalyzing free radical reactions leading to oxidative stress. In this report we discuss the biochemical changes observed after BOP exposure in rat blood and lung tissue, and propose a biochemical mechanism for free radical-induced oxidative stress that can potentially complicate the injury. Moreover, we observed that some antioxidants can interact with Hb oxidation products (oxy-, met- and oxoferrylHb) and act as prooxidants that can increase the damage rather than decrease it.

Antioxidant loading reduces oxidative stress induced by high-energy impulse noise (blast) exposure.

Detonation of explosives, firing of large caliber weapons and occupational explosions, professional or accidental, produce high-energy impulse noise (blast) waves characterized by a rapid rise in atmospheric pressure (overpressure) followed by gradual decay to ambient level. Exposure to blast waves causes injury, predominantly to the hollow organs such as ears and lungs. We have previously reported that blast exposure can induce free radical-mediated oxidative stress in the lung characterized by antioxidant depletion, lipid peroxidation, and hemoglobin (Hb) oxidation. In this study, we examined whether pre-loading, adequately fed rats, with pharmacological doses of antioxidants would reduce the response to blast. Sprague-Dawley rats weighing 300-350 g were loaded with either 800 IU vitamin E (VE), 1000 mg vitamin C (VC) or 25 mg lipoic acid (LA) for 3 consecutive days by gavage before exposure to blast. Both VE, and LA were dissolved in 2 ml corn oil, but VC in 2 ml water. After the 3-day antioxidant loading, the rats were divided into six groups (five rats per group), deeply anesthetized with sodium pentobarbital (60 mg/kg body weight), then exposed to a low-level blast (62+/-2 kPa peak pressure and 5 ms duration). A matched number of groups were sham exposed and served as controls. One hour after exposure, all rats were euthanized then blood, and lung tissue was analyzed. We found that antioxidant loading resulted in restored Hb oxygenation, and reduced lipid peroxidation. Lung tissue VE content was elevated after loading but VC did not change possibly due to their different bioavailability and saturation kinetics. These observations, suggest that brief antioxidant loading with pharmacological doses can reduce blast-induced oxidative stress, and may have occupational and clinical implications.

Free radical-mediated lung response to the monofunctional sulfur mustard butyl 2-chloroethyl sulfide after subcutaneous injection.

Vesicant-induced pathogenesis is initiated by rapid alkylation and cross-linking of DNA purine bases causing strand breaks leading subsequently to NAD depletion and cell death. We postulated that vesicants may also be associated with free radical-mediated oxidative stress distal to the site of exposure. To test this postulate in the lung, we injected 3 groups (n = 8) of 5-month-old, male, athymic, nude mice, weighing 30-35 g with a single subcutaneous (s.c.) injection (5 microliters/mouse) of butyl 2-chloroethyl sulfide (BCS), a monofunctional sulfur mustard analog. After 1, 24 and 48 h, we euthanized the treated mice along with 2 untreated control mice at each time point. We then pooled the control mice in one group (n = 6) and analyzed the lungs for biochemical indices of oxidative stress. We found that total lung weight was not altered after treatment, but wet/dry weight ratio decreased 18% (P less than 0.05) and hemoglobin content increased 50% and 36% at 1 and 24 h, respectively. The activity of glucose-6-phosphate dehydrogenase increased significantly, 40% at 1 and 24 h and 84% at 48 h and that of glutathione S-transferases was 60%, P less than 0.05 greater at all time points. Lipid peroxidation (estimated by the thiobarbituric acid test) and total protein content increased 3-fold and 2-fold, at 1 and 24 h, respectively. Total and oxidized glutathione contents were significantly elevated, 38% at 1 h and 64% at 24 h for the former and 45% at 24 h and 56% at 48 h for the latter. Because these changes are consistent with the cellular response to oxidative stress, we conclude that BCS injected subcutaneously, can cause changes in the lung possibly via a free radical-mediated mechanism.

Response of mouse brain to a single subcutaneous injection of the monofunctional sulfur mustard, butyl 2-chloroethyl sulfide (BCS)*.

Exposure to mustard-type vesicants results in alkylation of DNA and vesication. However, the biochemical mechanism for vesicant injury and whether it is localized or diffuse are not clear. We postulated that vesicant damage is mediated by free radicals, resulting in oxidative stress. These free radicals-mediated reactions may propagate systemically distal to the site of exposure. To test this hypothesis, we examined the effects of a single subcutaneous injection of the monofunctional sulfur mustard, butyl 2-chloroethyl sulfide (BCS), on the brain. We injected 3 groups (6 mice/group) of 5-month-old male, athymic, nude mice, weighing 30-35 g, subcutaneously with neat (undiluted) BCS (5 microliters/mouse). After 1, 24, and 48 h, we sacrificed the treated mice along with an untreated control group and analyzed the brains for biochemical markers of oxidative stress. Compared to untreated controls, the activity of glutathione peroxidase increased by 76%, P less than 0.005 at 24 h, and that of glutathione S-transferases by 25-37%, P less than 0.05 over the entire period. Total glutathione content in the brain was significantly lower, 17%, after 1 h and 23% after 24 h. We found also, concomitant with decreased glutathione, almost a 3-fold increase in susceptibility to lipid peroxidation. Because these changes are consistent with oxidative stress, we conclude that the effect of BCS administered subcutaneously may be translocated, reaching mouse brain, and causing oxidative stress.

Antioxidant mobilization in response to oxidative stress: a dynamic environmental-nutritional interaction.

In today's society, human activities and lifestyles generate numerous forms of environmental oxidative stress. Oxidative stress is defined as a process in which the balance between oxidants and antioxidants is shifted toward the oxidant side. This shift can lead to antioxidant depletion and potentially to biological damage if the body has an insufficient reserve to compensate for consumed antioxidants. This report focuses on the observation that oxidative stress resulting from inhalation of oxidant air pollutants mobilized vitamin E to the lung. A review of the literature showed that this mobilization is not limited to the lung; rather, a variety of situations in which oxidative stress occur can mobilize antioxidants. This antioxidant mobilization shows that a high antioxidant capacity in the body must be maintained for it to cope efficiently with environmental oxidative stress. Maintaining a high-antioxidant capacity in the body with the use of dietary supplementation was a convenient and acceptable method by test subjects, human or non-human. One mechanism that might explain the antioxidant mobilization is a dynamic interaction between environment and nutrition. In that mechanism, oxidative stress would alter certain bioactive molecules, followed by activation of signal transduction pathways that in turn would mobilize antioxidants to the target organ of the oxidant attack.

Influence of vitamin E and nitrogen dioxide on lipid peroxidation in rat lung and liver microsomes.

Rat lung and liver microsomes were used to examine the effects of dietary vitamin E deficiency on membrane lipid peroxidation. Microsomes from vitamin-E-deficient rats displayed increased lipid peroxidation in comparison to microsomes from vitamin-E-supplemented controls. The extent of lipid peroxidation, as determined by measurement of thiobarbituric acid reacting materials, was enhanced by addition of reduced iron and ascorbate (or NADPH). Rats fed a vitamin-E-supplemented diet and exposed to 3 ppm NO2 for 7 days did not exhibit increases in microsomal lipid peroxidation compared to air-breathing controls. However, increase were found in microsomes prepared from rats fed a vitamin-E-deficient diet and exposed to NO2. Lung microsomes from vitamin-E-fed rats contained almost 10 times as much vitamin E as liver microsomes when expressed in terms of polyunsaturated fatty acid content. The extent of lipid peroxidation was, in turn, considerably less in lung than in liver microsomes. Lipid peroxidation in lung microsomes from vitamin-E-deficient rats comparable to liver microsomes from vitamin-E-supplemented rats as was the content of vitamin E in these respective microsomal samples. A combination of vitamin E deficiency and NO2 exposure resulted in the greatest increases in lung and liver microsomal lipid peroxidation with the largest relative increases occurring in lung microsomes. An inverse relationship was found between the extent of lipid peroxidation and vitamin E content. Most of the peroxidation in lung microsomes appeared to proceed nonenzymatically whereas peroxidation in liver was largely enzymatic. Vitamin E appears to be assimilated by the lung during oxidant inhalation, but with dietary vitamin E deprivation, the margin for protection in lung may be less than in liver.

Jerusalem artichokes stimulate growth of broiler chickens and protect them against endotoxins and potential cecal pathogens.

Control of intestinal pathogens during the earliest phases of broiler production may be the best strategy for the reduction of human pathogens on processed broiler carcasses. The recent ban on antibiotics in poultry feed has served to focus much attention on alternative methods of controlling the gastrointestinal microflora. A field trial was conducted to evaluate the effect of the fructan-rich Jerusalem artichoke, or topinambur (administered as 0.5% topinambur syrup in drinking water), on cultural numbers of selected cecal bacteria (total aerobes, Enterobacteriaceae, Bdellovibrio spp., and Clostridium perfringens) and levels of bacterial endotoxins as well as on body weights and relative weights of organs (the pancreas and the bursa of Fabricius) of chickens in the first 35 days of life (with weekly investigations being conducted). One-day-old broiler chickens (Ross 308) were randomly assigned to experimental (with topinambur) and control (without topinambur) groups. They were allowed free access to a standard broiler diet without growth-promoting antibiotics. Topinambur treatment resulted in a significant increase (P < 0.01) in cecal counts of B. bacteriovorus, which parasitizes susceptible gram-negative pathogens. Topinambur led to significantly smaller numbers of total aerobes, Enterobacteriaceae, and C. perfringens as well as to reduced levels of endotoxins in the blood compared with those for control birds. Increased body weights resulting from topinambur consumption were observed on day 35 of the trial period (P < 0.05). The relative weights of the pancreas and the bursa of Fabricius, however, were higher (P < 0.05) for topinambur-treated broilers than for control birds at the ages of 14, 21, 28, and 35 days. These results indicate that a small amount of topinambur in broilers' drinking water has a beneficial effect on growth performance, reduces bacterial endotoxin levels, and suppresses potential pathogens in broilers' ceca.

Toxicity of five Sudanese plants to young ruminants.

The toxicity of 5 Sudanese plants credited with medicinal value for man, i.e. Citrullus colocynthis, Jatropha aceroides, J. glauca, Solanum dubium and Lagenaria siceraria, was studied by giving the dried or minced plants to Nubian goats, Desert sheep or Zebu calves by mouth or stomach tube. The clinical, haematological and pathological changes indicated that all five plants reduced the ability of the liver to synthesize protein, although there was no evidence of interference with the excretion of bilirubin. Kidney dysfunction and haemoconcentration also occurred. Citrullus colocynthis and Jatropha species in doses of 0.5 to 10 g per kg per day killed goats after dosing for periods ranging from 1 day to 2 weeks. Calves were less susceptible. The fruits and leaves of L. siceraria, in doses of 1 to 5 g per kg per day, caused death after a similar period but with less regularity. The seeds were less toxic. The fruits of S. dubium in doses of 2.5 to 10 g per kg per day killed goats in 2 to 5 days. Similar doses of the leaves caused deaths in 8 to 36 days. In sheep, both fruits and leaves required a longer period of dosing to cause death.