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Biomedical subjects

G F Combs

Publications and source records attributed to G F Combs.

At least 91 records · Page 5Linked to original sources
PubMed1982

Effects of dietary selenium and vitamin E on hepatic mixed-function oxidase activities and in vivo covalent binding of aflatoxin B1 in rats.

Male weanling fischer-344 rats were fed a selenium (Se)-vitamin E (VE) deficient Torula yeast basal diet or that diet supplemented with a graded levels of SE (0.2-6.0 ppm as Na2SeO3) or VE (100 iu/kg as all-rac-2-tocopheryl acetate), or both, for 4 or 6 weeks. Se deficiency and excess (6.0 ppm) markedly depressed in vivo covalent binding of aflatoxin (AFB1) to macromolecules in livers of rats killed 2 hours after an i.p. dose of 1 mg/kg tritiated AFB1. VE supplementation had no effect. Prior phenobarbital (PB) treatment generally decreased adducts without changing diet-related trends. Some hepatic enzyme capabilities were also measured. Cytochrome b5 content and cytochrome c reductase activity were unaffected by diet. VE increased cytochrome P-450 content, ethylmorphine N-demethylase and benz(alpha)pyrene hydroxylase activities; all these were unaffected by Se levels. Se deficiency and excess (but not VE deficiency) increased glucuronyl transferase. PB induction affected all diet groups and was more in agreement with MFO activity than transferase. Adduct formation was more consistently related to transferase activity than to MFO activities. The contrasting effects of SE and VE on AFB1 adducts in rats and chicks are discussed.

Aflatoxin B1↗
PubMed1982

Effects of dietary selenium and vitamin E on covalent binding of aflatoxin to chick liver cell macromolecules.

Day-old single comb white Leghorn chicks of both sexes maternally depleted in selenium (Se) and vitamin E (VE) were fed a low Se and VE-free semipurified basal diet or that diet supplemented with graded levels of Se (0.2 - 20.0 ppm as Na2SeO3) of VE (100 IU/g as all-rac-alpha-tocopheryl acetate), or both. At 14 days of age, chicks were given 1 mg/kg [3H] aflatoxin B1 (AFB1) i.p. and killed either 2 or 24 hours later. Covalent binding of AFB1 to liver DNA and RNA in chicks fed the basal diet was significantly greater than in chicks supplemented with Se or VE, or both. Phenobarbital treatment prior to administration of AFB1 decreased adduct formation in most groups, and abolished differences in adduct formation due to diet. These results suggest that combined Se-VE deficiency enhances activation or inhibits detoxification of AFB1 in vivo.

Aflatoxin B1↗
PubMed1982

Effect of selenium and vitamin E deficiency on nitrofurantoin toxicity in the chick.

The acute toxicity of nitrofurantoin was studied in the young chick deficient in selenium (Se) and/or vitamin E (E). This new and potentially valuable animal model proved to be very sensitive to the toxicity of this nitro drug. The 48-hour LD50 for nitrofurantoin decreased from 148 mg/kg in the Se- and E-supplemented chicks to 53 mg/kg in Se- and E-deficient chicks. The addition of Se (0.10 ppm as Na2SeO3) alone, but not E (100 IU/kg diet as dl-alpha-tocopheryl acetate) reduced the toxicity of nitrofurantoin, so that the LD50 for the chicks given Se alone was the same as the LD50 for the E- and Se-fed chicks. Se and E deficiency significantly decreased the Se-dependent glutathione peroxidase and the plasma tocopherol levels. Hepatic glutathione content, hepatic catalase and superoxide dismutase were unchanged by the dietary treatments. However, a toxic dose of nitrofurantoin significantly decreased hepatic glutathione content over time. These data support the concept that the toxicity of this drug may be mediated in part by an oxidative stress generated by the futile reductive metabolism of the parent compound.

Animals↗
PubMed1982

Dietary effects on selenite toxicity in the chick.

The toxicity of Na2SeO3 in diets containing torula (TY) or brewers' yeast (BY) compared to a corn-soy (CS) diet was investigated. Chick mortality caused by feeding 50 or 75 ppm Se as Na2SeO3 was significantly less with TY diets than with either BY or CS diets. The TY diet was also effective in reducing the depressing effect of Se on feed consumption and weight gain. Chicks fed 50 ppm Se in the TY diet accumulated the least amounts of Se in their livers and had only moderate hepatocellular fatty metamorphosis, whereas, those fed the same level of Se in BY diet accumulated the greater levels of Se and showed severe fatty metamorphosis. Partial or total replacement of TY (11%) with BY in the diet significantly increased mortality due to Se toxicity. Some protection against Se toxicity was associated with the ash fraction of TY. This may indicate that the protective effect of TY against Na2SeO3 toxicity is due at least in part to its mineral content.

Animals↗
PubMed1981

Relationship of selenium-dependent glutathione peroxidase activity and nutritional pancreatic atrophy in selenium-deficient chicks.

Experiments were conducted to determine the relationship of selenium-dependent glutathione peroxidase (SeGSHpx) activity to the onset of nutritional pancreatic atrophy (NPA) in chicks. Chicks produced from hens fed a low Se, low vitamin E practical diet had low activities of SeGSHpx in plasma and pancreas at hatching. The SeGSHpx activity remained at a low level before and during all stages of the onset of NPA. Selenium supplementation of the diet prevented NPA and resulted in significant elevations in SeGSHpx activity. Although the early stages of NPA are believed to involve mitochondrial swelling, no significant differences were found in rate of oxygen uptake, respiratory control index or adenosine diphosphate to oxygen ratio between pancreatic mitochondria isolated from Se-deficient or Se-adequate chicks. Improvements in maternal Se status significantly increased chick pancreatic SeGSHpx activity at hatching and delayed the onset of NPA in chicks fed a Se-deficient diet. A significant proportion of the second-generation Se- and vitamin E-depleted chicks used in these studies was found to grow at nearly normal rates when fed the Se-deficient diet. These chicks, designated as refractory to the growth-depressing effect of severe Se-deficiency, were biochemically deficient (i.e., had very low SeGSHpx activities) and showed NPA. It is concluded that the Se-responsive lesion which results in NPA in the chick is different from that which results in depressed growth.

Animals↗
PubMed1981

Effects on feed palatability of ingredients believed to contain unidentified growth factors for poultry.

The influences of several feedstuffs on the free-choice feeding behavior of Japanese quail, Single Comb White Leghorn (SCWL) chicks, broiler-type chicks, and SCWL hens were investigated. Each type of animal showed significant feeding preferences for diets containing practical feedstuffs popularly associated with unidentified growth factor (UGF) activities. Among these, diets containing menhaden meal and corn distillers' dried solubles were preferred most frequently. Results indicated that a component of the UGF activities of practical feedstuffs may be an increase in feed palatability. Controlled feeding diets containing menhaden meal to Japanese quail demonstrated a typical UGF effect in addition to a palatability effect.

Animal Feed↗
PubMed1981

Impaired vitamin E status of chicks fed T-2 toxin.

Experiments were conducted to evaluate the toxicity of dietary T-2 toxin (4,15-diacetoxy-8-(3-methylbutyryloxy)-12,13-epoxy-delta 9-tricothecen-3-ol) in young pullets. Growth of day-old chicks fed a practical-type diet containing the toxin was described by the following function: Y = .152 + 58.497e(.305X1-.005X2(1.66); where Y = gain as percentage starting weight per week; X1 is time in weeks and O less than or equal to X2 is T-2 content of diet in ppm and O less than or equal to X2 less than or equal to 15. Chicks chronically exposed to the toxin showed compensatory growth upon its removal from the diet; however, latent effects on energy utilization were observed. Lesions of the oral mucosa produced by T-2 toxin showed spontaneous remission after about 14 days. T-2 toxin consistently produced depressed concentrations of vitamin E in plasma. Addition of micelle-promoting compounds (taurocholic, monoolein, and oleic acids) alleviated depressions in both plasma vitamin E and growth.

Animals↗
PubMed1981

Blood ionized calcium cycles in the chicken.

Changes in blood ionized calcium concentration (Ca++) appear to be dependent on the physiological state of the chicken. In the laying hen, blood Ca++ levels were affected by the ovulatory cycle; Ca++ was elevated when the shell gland was empty, declined following entry of an egg into that organ, and reached a minimum level approximately 16 hr prior to the subsequent oviposition. Pullets not in laying condition had blood Ca++ that varied with the photoperiod and/or rate of feed intake. In those pullets, blood Ca++ levels were depressed during the 9.5 hr of light, then rose in plateaued during the dark period. These studies indicate that blood Ca++ in laying hens is affected by the reproductive state first and the photoperiod and/or pattern of feed intake second.

Animals↗
PubMed1981

Influences of dietary vitamin E and selenium on the oxidant defense system of the chick.

The effects of dietary vitamin E and selenium on the oxidant defense system (glutathione peroxidase, catalase, glutathione reductase, reduced glutathione, and superoxide dismutase) were investigated in the chick. Two-week-old chicks were reared using a vitamin E-free, low-selenium, semipurified basal diet alone or supplemental with vitamin E (100 IU/kg) and/or selenium (.10 ppm). Whereas vitamin E sustained chick growth, survival, and protection from exudative diathesis (ED), it did not significantly affect the enzymatic components of the oxidant defense system. Dietary selenium promoted chick growth and protection against ED in the absence of vitamin E and sustained glutathione peroxidase activity in several tissues. The latter effect was associated with decreases in reduced glutathione concentrations observed in liver and blood. Catalase and superoxide dismutase activities were increased in liver and brain in selenium deficiency. Glutathione reductase activities in liver, kidney, lung, and brain were not affected by diet.

Animals↗
PubMed1981

Influence of dietary selenium on performance, tissue selenium content, and plasma concentrations of selenium-dependent glutathione peroxidase, vitamin E, and ascorbic acid in ducklings.

Low-selenium corn-soya diets (.04 ppm Se) supplemented with 0, .1, or .2 ppm was selenium (as Na2SeO3), in the presence or absence of 10 IU of supplemental vitamin E per kilogram, were fed to progeny of selenium-depleted breeder ducks. Ducklings from nondepleted breeders received selenium-adequate diets supplemented with 0, .1, or 1.0 ppm selenium from Na2SeO3. High mortalityyy, extensive muscle necrosis, and depressed early weight gain occurred in ducklings fed the low-selenium diets without added selenium. These effects were not prevented by supplemental vitamin E. None of the above manifestations of selenium deficiency were observed in ducklings fed the low-selenium diets supplemented with .1 or .2 ppm selenium. The addition of up to 1.0 ppm selenium to the adequate-selenium diet had no significant effect on mortality or weight gain. The selenium content of kidney, liver, and muscle increased with the addition of .1 ppm selenium to the low-selenium diet. Relatively small increases in tissue selenium concentrations resulted from the addition, to either diet, or levels of selenium in excess of the nutritional requirement. Glutathione peroxidase in plasma varied directly with selenium additions to the low-selenium diets. Plasma vitamin E increased as dietary vitamin E and selenium were increased. Dietary treatment had no significant effect on the concentration of ascorbic acid in plasma.

Animals↗
PubMed1980

Effect of selenium on appetite in the selenium-deficient chick.

Experiments were conducted to determine the initial effects of oral selenium administration on selenium-deficient chicks. Administration of 5 microgram selenium as seleno-DL-methionine increased voluntary feed consumption within 2-3 hours, whereas selenite did not have a significant effect until 3-4 hours. Spontaneous activity, body weight gain and plasma glucose concentration increased 6-8 hours after selenium administration. The earliest response in the specific activity of selenium-dependent glutathione peroxidase occurred in plasma at 8 hours and in liver at 24 hours after selenium administration. The onset of pancreatic atrophy, however, was not affected by the level of feed intake suggesting that the effect of selenium upon appetite may be distinct from the involvement of selenium in nutritional pancreatic atrophy and fibrosis.

Animals↗
PubMed1980

Influence of selenium, vitamin E, and ethoxyquin on lipid peroxidation in muscle tissues from fowl during low temperature storage.

The influences of various factors which affect the selenium-vitamin E status of laying hens on lipid peroxidation in muscle tissues during low temperature storage were studied. Laying hens from 32 to 56 weeks of age were fed low selenium and low vitamin E practical diets supplemented with different levels of Na2SeO3, d1-alpha-tocopherol acetate, ethoxyquin, and/or peroxidized corn oil. Vitamin E status as indicated by plasma vitamin E activity was improved by supplements of vitamin E, selenium, or ethoxyquin. Selenium status as indicated by plasma selenium-dependent glutathione peroxidase activity was improved by selenium supplementation. Incorporation of peroxidized corn oil into diets did not depress plasma vitamin E but increased plasma glutathione peroxidase when those diets contained supplemental selenium. Lipid peroxidation as indicated by the 2-thiobarbituric acid (TBA) method in muscle samples held at -20 C for up to 270 days was reduced by dietary selenium in M. pectoralis when corn oil was fed. Supplemental vitamin E or ethoxyquin reduced TBA values developed in M. gastrocnemius. Results indicate that dietary selenium and other factors affecting selenium status may be useful in retarding the development of oxidative rancidity in frozen poultry products.

Animals↗