Showing papers on "Ascorbic acid published in 1987"

Water Pollution and Fish Physiology

Abstract: Some Introductory Concepts Types of Water Pollution The Relationship Between Aquatic Toxicology and Fish Physiology Levels of Biological Organization Importance of Dose and Duration of Exposure Stress Toxic Mode of Action Environmental Hypoxia Minimum Levels of Oxygen Required for Fish Life Interaction of Hypoxia and Toxicity of Pollutant Chemicals Gill vs. Cutaneous Respiration Adjustments in Ventilation Adjustments by the Gills to Hypoxia Transport of Oxygen by the Blood Cardiovascular Changes During Hypoxia Respiratory Regulation and Conformity Anaerobic Metabolism Swimming Speed Behavior Blood and Urine Histopathology Acclimation to Hypoxia Respiratory and Cardiovascular Responses Overview of Normal Respiratory Physiology Histopathology of Gill Lamellae Exposed to Pollutants Ventilation Changes in Response to Pollutants Physiological Mechanisms of Changes in Ventilation Circulatory Physiology Cardiac Responses to Pollutants Hematology Fish Blood Cells and their Measurement Chemicals that Cause Anemia Chemicals Causing an Increase in Hematological Variables Uptake, Accumulation, Biotransformation, and Excretion of Xenobiotics Uptake from the Environment Transport Within the Fish of Metals and Organics Accumulation of Metals in Different Organs Regulation of Metal Concentration Glutathione and Metal Detoxification Involvement of Metallothionein in Metal Accumulation and Acclimation to Metals Bioconcentration of Organic Pollutants Biotransformation of Organic Contaminants Excretion of Organic Contaminants Liver Structure of Liver Alterations of Liver/Somatic Index Histopathological Effects of Pollutants Major Functions of Liver Effects of Pollutants on Liver Function Ascorbic Acid and Pollutant Exposure Osmotic and Ionic Regulation Effects of Pollutants on Osmotic and Ionic Regulation Mucus Chloride Cell Proliferation Some Summary Comments Regarding Osmoregulatory and Electrolyte Alterations Physiological Energetics General Concepts Methods for Measuring Energy Expenditure in Fish Effects of Metals on Metabolic Rate Gill Tissue Metabolism: Effects of Metals and Possible Relation of Gill Metabolism to Whole-Body Metabolic Rate Effects of Pesticides on Whole-Body and Individual Tissue Respiration Methods Applicable to Measurement of Energy Expenditure in the Field Effects of Pollutants on Larval and Juvenile Growth Swimming Performance Changes in Carbohydrate, Lipid, and Protein Energy Stores Alterations in Cellular Enzyme Activity, Antioxidants, Adenylates, and Stress Proteins Some Comments About Enzyme Methodology Alterations in Cellular Enzyme Activity from Metal Exposure Enzyme Effects from Organic Chemicals Concluding Remarks on Enzyme Effects Antioxidants Adenylates Stress Proteins Acid Pollution Spawning Embryonic Development and Hatching Larvae from Hatching Through Swim-Up Juvenile and Adult: Acid-Base Balance and Electrolyte Changes from Acute Exposures Juvenile and Adult: Blood Changes from Chronic Exposures Hormonal Responses Adults: Ventilation and Blood Gases Oxygen Consumption, Swimming Performance, and Swimbladder Inflation Behavior Concluding Comment The Immune System Effects of Pollutants on Immune Function Hormonal Modulation of Immune Response Behavior and Nervous System Function Locomotor Activity Avoidance of or Attractance to Waterborne Chemicals Sensory Receptors Feeding and Predator-Prey Behavior Aggression Learning Optomotor Response Acetylcholinesterase Concluding Comments Reproduction Overview of Fish Reproductive Physiology Action of Pollutants on Reproductive Function Use of Physiological and Biochemical Measures in Pollution Biology Water Quality Criteria Biomonitoring of Fish in the Field and Mesocosms Early Warning Systems Index Each chapter includes an introduction and/or overview and a list of relevant references.

Free radical tissue damage: protective role of antioxidant nutrients.

Abstract: Highly reactive molecules called free radicals can cause tissue damage by reacting with polyunsaturated fatty acids in cellular membranes, nucleotides in DNA, and critical sulfhydryl bonds in proteins. Free radicals can originate endogenously from normal metabolic reactions or exogenously as components of tobacco smoke and air pollutants and indirectly through the metabolism of certain solvents, drugs, and pesticides as well as through exposure to radiation. There is some evidence that free radical damage contributes to the etiology of many chronic health problems such as emphysema, cardiovascular and inflammatory diseases, cataracts, and cancer. Defenses against free radical damage include tocopherol (vitamin E), ascorbic acid (vitamin C), beta-carotene, glutathione, uric acid, bilirubin, and several metalloenzymes including glutathione peroxidase (selenium), catalase (iron), and superoxide dismutase (copper, zinc, manganese) and proteins such as ceruloplasmin (copper). The extent of tissue damage is the result of the balance between the free radicals generated and the antioxidant protective defense system. Several dietary micronutrients contribute greatly to the protective system. Based on the growing interest in free radical biology and the lack of effective therapies for many of the chronic diseases, the usefulness of essential, safe nutrients in protecting against the adverse effects of oxidative injury warrants further study.

Differentiation of axon-related Schwann cells in vitro. I. Ascorbic acid regulates basal lamina assembly and myelin formation

Abstract: Rat Schwann cells cultured with dorsal root ganglion neurons in a serum-free defined medium fail to ensheathe or myelinate axons or assemble basal laminae. Replacement of defined medium with medium that contains human placental serum (HPS) and chick embryo extract (EE) results in both basal lamina and myelin formation. In the present study, the individual effects of HPS and EE on basal lamina assembly and on myelin formation by Schwann cells cultured with neurons have been examined. Some batches of HPS were unable to promote myelin formation in the absence of EE, as assessed by quantitative evaluation of cultures stained with Sudan black; such HPS also failed to promote basal lamina assembly, as assessed by immunofluorescence using antibodies against laminin, type IV collagen, and heparan sulfate proteoglycan. The addition of EE or L-ascorbic acid with such HPS led to the formation of large quantities of myelin and to the assembly of basal laminae. Pretreatment of EE with ascorbic acid oxidase abolished the EE activity, whereas trypsin did not. Other batches of HPS were found to promote both basal lamina and myelin formation in the absence of either EE or ascorbic acid. Ascorbic acid oxidase treatment or dialysis of these batches of HPS abolished their ability to promote Schwann cell differentiation, whereas the subsequent addition of ascorbic acid restored that ability. Ascorbic acid in the absence of serum was relatively ineffective in promoting either basal lamina or myelin formation. Fetal bovine serum was as effective as HPS in allowing ascorbic acid (and several analogs but not other reducing agents) to manifest its ability to promote Schwann cell differentiation. We suggest that ascorbic acid promotes Schwann cell myelin formation by enabling the Schwann cell to assemble a basal lamina, which is required for complete differentiation.

Rationale and Strategies for Chemoprevention of Cancer in Humans

Abstract: The potential for chemical intervention (chemoprevention) as a means of halting or delaying the process of carcinogenesis is assessed as a strategy for reducing the incidence of human cancer. The process of carcinogenesis is dissected into its constituent steps, thereby exposing sites for intervention. These sites are then critically discussed with regard to the existence of chemicals active at these sites using data gained from the laboratory and from epidemiological studies, intrinsic problems or advantages associated with intervention at specific sites in the carcinogenic process, and practical aspects of intervention in humans. The design and potential long-term positive and negative consequences of chemoprevention clinical trials are critically discussed, with the objective of exposing the major differences that exist between clinical trials in cancer chemoprevention and those in cancer chemotherapy. Results of completed prevention trials and details of ongoing trials are presented and discussed. Based on the laboratory, epidemiological, and clinical evidence presented, it is concluded that chemoprevention offers excellent prospects as a means of reducing cancer incidence. Among currently available agents, the retinoids possess the best combination of properties. However, much more research is needed to optimize drugs and protocols and to develop interim end points for assessing response. The authors finally caution that overambitious claims for the prospects for chemoprevention may lead to reduced emphasis on the need for changes in life-style (principally in smoking and diet) that are viewed as having the greatest potential for reducing cancer incidence.

Initiation of lipid peroxidation in biological systems

Abstract: The direct oxidation of PUFA by triplet oxygen is spin forbidden. The data reviewed indicate that lipid peroxidation is initiated by nonenzymatic and enzymatic reactions. One of the first steps in the initiation of lipid peroxidation in animal tissues is by the generation of a superoxide radical (see Figure 16), or its protonated molecule, the perhydroxyl radical. The latter could directly initiate PUFA peroxidation. Hydrogen peroxide which is produced by superoxide dismutation or by direct enzymatic production (amine oxidase, glucose oxidase, etc.) has a very crucial role in the initiation of lipid peroxidation. Hydrogen peroxide reduction by reduced transition metal generates hydroxyl radicals which oxidize every biological molecule. Hydrogen peroxide also activates myoglobin, hemoglobin, and other heme proteins to a compound containing iron at a higher oxidation state, Fe(IV) or Fe(V), which initiates lipid peroxidation even on membranes. Complexed iron could also be activated by O2- or by H2O2 to ferryl iron compound, which is supposed to initiate PUFA peroxidation. The presence of hydrogen peroxide, especially hydroperoxides, activates enzymes such as cyclooxygenase and lipoxygenase. These enzymes produce hydroperoxides and other physiological active compounds known as eicosanoids. Lipid peroxidation could also be initiated by other free radicals. The control of superoxide and perhydroxyl radical is done by SOD (a) (see Figure 16). Hydrogen peroxide is controlled in tissues by glutathione-peroxidase, which also affects the level of hydroperoxides (b). Hydrogen peroxide is decomposed also by catalase (b). Caeruloplasmin in extracellular fluids prevents the formation of free reduced iron ions which could decompose hydrogen peroxide to hydroxyl radical (c). Hydroxyl radical attacks on target lipid molecules could be prevented by hydroxyl radical scavengers, such as mannitol, glucose, and formate (d). Reduced compounds and antioxidants (ascorbic acid, alpha-tocopherol, polyphenols, etc.) (e) prevent initiation of lipid peroxidation by activated heme proteins, ferryl ion, and cyclo- and lipoxygenase. In addition, cyclooxygenase is inhibited by aspirin and nonsteroid drugs, such as indomethacin (f). The classical soybean lipoxygenase inhibitors are antioxidants, such as nordihydroguaiaretic acid (NDGA) and others, and the substrate analog 5,8,11,14 eicosatetraynoic acid (ETYA), which also inhibit cyclooxygenase (g). In food, lipoxygenase is inhibited by blanching. Initiation of lipid peroxidation was derived also by free radicals, such as NO2. or CCl3OO. This process could be controlled by antioxidants (e).(ABSTRACT TRUNCATED AT 400 WORDS)

Anthocyanins as food colorants —a review

Abstract: A number of factors affecting anthocyanin stability and color are discussed in this review. The anthocyanins are probably the most spectacular of plant pigments since they are responsible for most of the red, purple and blue pigmentation of flowers, fruits and vegetables. However, because of their highly reactive nature, anthocyanins readily degrade, or react with other constituents in the media, to form colorless or brown colored compounds. The presence of an ox-onium ion adjacent to carbon 2 makes the anthocyanins particularly susceptible to nucleophilic attack by such compounds as sulfur dioxide, ascorbic acid, hydrogen peroxide and even water. Loss of anthocyanin pigmentation also occurs in the presence of oxygen and various enzymes, and as a result of high temperature processing. A certain degree of pigment stabilization may be conferred by acylation with various organic acids, copigmentation, self-association and/or metal chelation. In addition, pH has a marked effect on anthocyanin stability, and on the color of media containing these pigments. A number of anthocyanin-rich sources have been investigated for their potential as commercial pigment extracts. Although their application is primarily limited to acidic media, continued research on the chemistry of anthocyanins may lead to application and stabilization of these pigments in a wider variety of food products.

Physiological concentrations of glucocorticoids stimulate formation of bone nodules from isolated rat calvaria cells in vitro.

Abstract: Isolated rat calvaria cells plated at low density in medium supplemented with ascorbic acid and organic phosphate form discrete three-dimensional mineralized nodules having the characteristics of bone. We have studied the effects of glucocorticoids on the formation of bone nodules by these cell populations. Cells isolated from 21-day-old fetal rat calvaria were maintained in vitro for up to 27 days. Dexamethasone (Dex) induced a dose-related increase in the number of nodules formed, with a peak at 10 nM and a half-maximal response at about 1 nM. Dex (10 nM) also significantly increased the size of bone nodules formed (P less than 0.002). High concentrations of Dex (1 microM) did not increase nodule number. In cells in primary culture maintained in medium containing 10 nM Dex, the increase in nodule number was 50-100% over the control value. The effect of Dex was much greater in first subculture cells, where the number of nodules was 600-800% higher than the control value. Dishes collected and quantitated from 12-27 days showed that nodule formation ceased between 15 and 18 days in cultures without Dex, whereas in the presence of Dex the number of nodules increased up to 27 days. Addition of 10 nM Dex only during specific periods resulted in significantly more nodules than in control cultures, but significantly fewer nodules than in cultures constantly exposed to Dex. Cell population doubling times during log phase growth were unaltered, but a significant increase in saturation density (P less than 0.001) was observed with 10 nM Dex. Hydrocortisone also caused an increase in the number of nodules formed, with a maximal effect of 50 nM and a half-maximal response at 8 nM. The results indicate that physiological levels of glucocorticoids stimulate bone nodule formation in long term cell culture by increasing the number of cells forming bone nodules and that maximization of the stimulatory effect of glucocorticoids on bone formation may require constant exposure to low levels of the hormone.

Cysteamine Therapy for Children with Nephropathic Cystinosis

Abstract: We treated 93 children with nephropathic cystinosis with oral cysteamine (mean dose, 51.3 mg per kilogram of body weight per day) for up to 73 months. This agent is known to be effective in depleting cells of cystine. In our study, the mean cystine depletion from leukocytes was 82 percent. A historical control group of 55 children received either ascorbic acid (27 children) or placebo (28). At age six, 2 of 17 controls had a serum creatinine level less than 1.0 mg per deciliter, as compared with 17 of 27 patients treated with cysteamine for at least one year (odds ratio, 12.8; 95 percent confidence interval, 2.1 to 33.9). At the end of the study, creatinine clearance was higher in the cysteamine group than in the control group (38.5 vs. 29.7 ml per minute per 1.73 m2; 95 percent confidence limits on the difference, 1.8 and 15.8), even though the cysteamine group was on average 1.4 years older than the control group. Cysteamine also improved growth; those in the cysteamine group between two and three years of age grew at 93 percent of the normal velocity, as compared with 54 percent in the control group. Fourteen percent of the patients could not tolerate the taste and smell of cysteamine. Concurrent controls treated in a blinded fashion with a placebo were not included in this study. With this limitation in mind, we conclude that oral cysteamine, by depleting cells of cystine, helps maintain renal glomerular function, improves growth, and constitutes the current treatment of choice for nephropathic cystinosis.

Superoxide-dependent and ascorbate-dependent formation of hydroxyl radicals from hydrogen peroxide in the presence of iron. Are lactoferrin and transferrin promoters of hydroxyl-radical generation?

Abstract: Apo-lactoferrin and apo-transferrin protect against iron-ion-dependent hydroxyl-radical (.OH) generation from H2O2 in the presence of superoxide radicals or ascorbic acid at pH 7.4, whether the necessary iron is added as ionic iron or as ferritin. Iron-loaded transferrin and lactoferrin [2 mol of Fe(III)/mol] show no protective ability, but do not themselves accelerate .OH production unless chelating agents are present in the reaction mixture, especially if the proteins are incorrectly loaded with iron. At acidic pH values, the protective ability of the apoproteins is diminished, and the fully iron-loaded proteins can release some iron in a form able to accelerate .OH generation. The physiological significance of these observations is discussed.

Estrogen carcinogenesis in Syrian hamster tissues: role of metabolism.

Abstract: Evidence for a role of estrogen metabolism in hormonal carcinogenesis was obtained with the Syrian hamster as an in vivo model system. Both natural and synthetic estrogens are capable of inducing a high incidence of renal carcinomas in this species. A high incidence of hepatocellular carcinomas can also be induced in the hamster with synthetic estrogens such as ethinyl estradiol or diethylstilbestrol, provided alpha-naphthoflavone (ANF) is present in the diet. Although steroid receptor-mediated hormonal events appear to be intimately involved in the process of in vivo cell transformation of both tissues, certain observations strongly suggest that nonhormonal events are also important. Despite their potent estrogenic activity at the doses used, ethinyl estradiol and alpha-zearalanol induce relatively low renal tumor incidences after 9.0 and 10.0 months of continuous treatment, respectively. A role for the metabolism of estrogens to reactive intermediates is also suggested by studies showing estrogen-induced renal tumorigenesis can be partially inhibited by concomitant administration of ANF or ascorbic acid. Consistent with this is the general correlation between the amount of catechol estrogen formed by a compound, as mediated by estrogen 2-/4-hydroxylase, and renal carcinogenicity data. Recently, additional supporting evidence has been obtained from studies involving the irreversible binding of reactive metabolites of steroidal or stilbene estrogens to hamster liver microsomal proteins.

Measurement of Enzymatic Browning at Cut Surfaces and in Juice of Raw Apple and Pear Fruits

Abstract: Reflectance procedures were developed to measure the extent of enzymatic browning at cut surfaces and in the raw juice of apple and pear fruits. Reflectance L and a measurements, made at transversely cut surfaces of plugs bored from fruit halves, were linear or bilinear with log time and related to the extent of browning in six apple cultivars. With apple and pear juices, tristimulus values changed linearly with time in samples undergoing browning. Differences between initial and final tristimulus values were better indices of browning than the slopes of time curves. The suitability of these procedures for evaluating the effectiveness of browning inhibitors was demonstrated with SO2 and ascorbic acid treatments.

Effective chelation of iron in beta thalassaemia with the oral chelator 1,2-dimethyl-3-hydroxypyrid-4-one.

Abstract: The main iron chelator used for transfusional iron overload is desferrioxamine, which is expensive, has toxic side effects, and has to be given subcutaneously. An orally active iron chelator is therefore required. The effects of oral 1,2-dimethyl-3-hydroxypyrid-4-one on urinary iron excretion were studied in eight patients who had received multiple transfusions: four had myelodysplasia and four beta thalassaemia major. Different daily doses of the drug up to 100 mg/kg/day, alone or in combination with ascorbic acid, were used. In three patients with thalassaemia the effect of the drug was compared with that of subcutaneous desferrioxamine at the same daily dose. In all eight patients a single dose of oral 1,2-dimethyl-3-hydroxypyrid-4-one resulted in substantial urinary iron excretion, mainly in the first 12 hours. Urinary iron excretion increased with the dose and with the degree of iron loading of the patient. Giving two or three divided doses over 24 hours resulted in higher urinary iron excretion than a single dose of the same amount over the same time. In most patients coadministration of oral ascorbic acid further increased urinary iron excretion. 1,2-Dimethyl-3-hydroxypyrid-4-one caused similar iron excretion to that achieved with subcutaneous desferrioxamine at a comparable dose. In some cases the iron excretion was sufficiently high (maximum 99 mg/day) to suggest that a negative iron balance could be easily achieved with these protocols in patients receiving regular transfusions. No evidence of toxicity was observed on thorough clinical examination or haematological and biochemical testing in any of the patients. None of the patients had any symptoms that could be ascribed to the drug. These results suggest that the oral chelator 1,2-dimethyl-3-hydroxypyrid-4-one is as effective as subcutaneous desferrioxamine in increasing urinary iron excretion in patients loaded with iron. Its cheap synthesis, oral activity, and lack of obvious toxicity at effective doses suggest that it should be developed quickly and thoroughly tested for the management of transfusional iron overload.

The effects of fruit juices and fruits on the absorption of iron from a rice meal.

Abstract: The effects of the chemical composition of fruit juices and fruit on the absorption of iron from a rice (Oryza sativa) meal were measured in 234 parous Indian women, using the erythrocyte utilization of radioactive Fe method. The corrected geometric mean Fe absorptions with different juices varied between 0.040 and 0.129, with the variation correlating closely with the ascorbic acid contents of the juices (rs 0.838, P less than 0.01). Ascorbic acid was not the only organic acid responsible for the promoting effects of citrus fruit juices on Fe absorption. Fe absorption from laboratory 'orange juice' (100 ml water, 33 mg ascorbic acid and 750 mg citric acid) was significantly better than that from 100 ml water and 33 mg ascorbic acid alone (0.097 and 0.059 respectively), while Fe absorption from 100 ml orange juice (28 mg ascorbic acid) was better than that from 100 ml water containing the same amount of ascorbic acid (0.139 and 0.098 respectively). Finally, Fe absorption from laboratory 'lemon juice' (100 ml orange juice and 4 g citric acid) was significantly better than that from 100 ml orange juice (0.226 and 0.166 respectively). The corrected geometric mean Fe absorption from the rice meal was 0.025. Several fruits had little or no effect on Fe absorption from the meal (0.013-0.024). These included grape (Vitis vinifera), peach (Prunus persica), apple (Malus sylvestris) and avocado pear (Persea americana). Fruit with a mild to moderate enhancing effect on Fe absorption (0.031-0.088) included strawberry (Fragaria sp.) (uncorrected values), plum (Prunus domestica), rhubarb (Rheum rhaponticum), banana (Musa cavendishii), mango (Mangifera indica), pear (Pyrus communis), cantaloup (Cucumis melo) and pineapple (Ananas comosus) (uncorrected values). Guava (Psidium guajava) and pawpaw (Carica papaya) markedly increased Fe absorption (0.126-0.293). There was a close correlation between Fe absorption and the ascorbic acid content of the fruits tested (rs 0.738, P less than 0.0001). There was also a weaker but significant correlation with the citric acid content (rs 0.55, P less than 0.03). Although this may have reflected a direct effect of citric acid on Fe absorption, it should be noted that fruits containing citric acid also contained ascorbic acid (rs 0.70, P less than 0.002).(ABSTRACT TRUNCATED AT 400 WORDS)

Interaction between oxygen radicals and gastric mucin.

Abstract: The gastrointestinal epithelium is continuously exposed to reactive oxygen metabolites that are generated within the lumen. In spite of this exposure, the healthy epithelium appears unaffected, suggesting efficient mechanisms for protection against these potentially cytotoxic oxidants. The objective of this study is to characterize the interaction between purified gastric mucin and hydroxyl radicals generated from the interaction between ferric iron and ascorbic acid. We found that both native and pronase-treated mucin effectively scavenged hydroxyl radical and that the scavenging properties were not significantly different. The effective concentration of mucin required for a 50% reduction in malondialdehyde production was approximately 10 mg/ml for both native and pronase-treated mucin. In addition, the iron-ascorbic system produced a dramatic decrease (greater than 50%) in the specific viscosity of mucin that was inhibited by catalase, deferoxamine, and mannitol. Superoxide dismutase had no effect. These data suggest that hydroxyl radicals derived from the iron-catalyzed decomposition of hydrogen peroxide are responsible for the depolymerization of native mucin. We propose that mucin may provide protection to the surface epithelium of the gastrointestinal tract by scavenging oxidants produced within the lumen; however, it does so at the expense of its viscoelastic properties.

Covalent Binding of Acetaldehyde to Proteins: Participation of Lysine Residues

Abstract: The results of this study demonstrate that lysine is the major amino acid participating in the binding of acetaldehyde to proteins. The formation of both stable and unstable acetaldehyde-albumin adducts was shown to occur via the reaction of acetaldehyde with lysine residues. This conclusion was based on the following experimental evidence: (a) the ratio of stable to unstable adducts of bovine serum albumin was similar to that observed for polylysine; (b) acetylation of albumin markedly reduced acetaldehyde binding; (c) the radio-activity profiles (obtained by high-performance liquid chromatographic analysis) of [14C]acetaldehyde modified amino acids hydrolyzed from total and stable adducts of albumin were nearly identical to those of polylysine or alpha-t-boc-lysine. Analysis of stable adducts of albumin indicated two major modified lysine residues; one residue was much more acidic and the other more basic than unmodified lysine. Unstable adducts were shown to be Schiff bases since NaBH4 treatment resulted in the formation of N-ethyllysine residues. The reducing agents, NaCNBH3 and ascorbic acid, both increased stable adduct formation via increased binding to lysine residues; however, a different elution profile of modified lysine residues was observed for these reducing agents. NaCNBH3 increased the formation of N-ethyllysine residues exclusively, whereas ascorbate increased the formation of the acidic adduct of lysine and also caused the formation of an additional modified lysine residue which was present only in the ascorbate-treated polypeptides. In addition to their detection by radioactivity measurements, the acetaldehyde-lysine adducts could also be detected by the fluorescence of their ophthalaldehyde derivatives.(ABSTRACT TRUNCATED AT 250 WORDS)

Continuous and stopped flow EPR spectrometer based on a loop gap resonator

Abstract: A continuous and stopped flow EPR spectrometer based on a new loop gap resonator operating at X band is described. The important features of the instrument are: (1) very small amounts of material are consumed in both stopped and continuous flow modes of operation, (2) dead times on the order of 4 ms for stopped flow and 1 ms for continuous flow are realized with a very narrow age distribution in the sample compartment, and (3) the dead times and, hence, sample age are highly reproducible and independent of viscosity due to the use of a positive displacement syringe ram. The performance of the instrument is evaluated using the decay of ascorbate radical generated by Ce(iv) oxidation and reduction of nitroxides by ascorbic acid.

Safety of High‐level Vitamin C Ingestion

Abstract: Vitamin C is widely consumed as a dietary supplement, ingested either as a single nutrient or in combination with other vitamins and minerals. Stewart et al. reported that 35.1% of the adult U.S. population ingested a vitamin C supplement, with a median intake of 333% of the Recommended Dietary Allowance (RDA) and 28 times the RDA at the 95th percentile. Further, gram amounts of ascorbic acid are suggested for treatment and /or prevention of a wide array of health aberrations. Concern about the safety of these practices has been addressed in recent reviews.

Biochemical analysis of bovine follicular fluid: albumin, total protein, lysosomal enzymes, ions, steroids and ascorbic acid content in relation to follicular size, rank, atresia classification and day of estrous cycle.

Abstract: To investigate some biochemical changes during bovine follicle development, ovaries were obtained from cyclic heifers (7 to 11 heifers/d on each day of the 21-d estrous cycle; N = 152). Follicular fluid from the two largest follicles from both ovaries and a pool from small follicles (N = 30/cow) were collected from each animal and analyzed for ionic, enzymatic and endocrine changes in relation to day of the estrous cycle, follicle size, rank and atretic or growing status. Follicular fluid alkaline phosphatase activity and ascorbate concentrations were highest in all follicular sizes during the earlier portion of the estrous cycle (d 1 to 12; P less than .05), then decreased to the lowest levels (d 13 to 21). As follicular size (diameter) increased lactate dehydrogenase (LDH), acid and alkaline phosphatase activity was reduced in follicular fluid (P less than .05). Alkaline phosphatase and LDH activity tended to be increased in atretic follicles (P less than .10), and was correlated with increased progesterone and androgen concentrations of follicular fluid (r = .4, P less than .05). Both albumin and total protein concentrations decreased as follicular diameter increased (P less than .05). Sodium concentrations in follicular fluid were greater in growing-antral than atretic follicles, and increased with follicular enlargement (P less than .05). Follicular potassium concentrations increased as the estrous cycle progressed (P less than .05), and tended to be elevated in atretic follicles (nonsignificant). Both Ca and Mg concentrations increased with follicular enlargement (P less than .05). Dehydroepiandrosterone and testosterone were the predominant androgens in follicular fluid (androstenedione, the lowest concentration); their concentration decreased with follicle development (P less than .05), but were quite variable. Estradiol was increased in growing follicles (P less than .01). Estrone and estradiol concentrations increased as ovulation approached, particularly in small follicles (less than or equal to 4 mm diameter). Changes of biochemical components found in follicular fluid that relate to the growth and atresia process may provide a more sensitive and accurate method to classify follicle status, and thus aid in understanding the complexity of events associated with maturation of the bovine follicle and oocyte.