Organoleptic characteristics and compositional profile of meat of growing Japanese quail fed different levels of poultry byproducts compost.

The poultry industry generates a lot of waste, including dead birds, manure, and poultry litter. Poultry waste should never be disposed of improperly because it can seriously harm the environment. The waste can be recycled as a feedstock for use in poultry feed by composting the litter and deceased birds. The compositional profile and organoleptic properties of the meat of growing Japanese quail were examined over the course of a 4-week trial to ascertain the effect of adding compost to the diet. In a completely randomized design (CRD), 1200 newly hatched quail chicks (Coturnix coturnix japonica) were divided into five treatment groups (diets with 0, 2.5, 5, 7.5, and 10% compost), each consisting of 40 birds with six replicates. The addition of compost to the diet had no noticeable effects on the organoleptic qualities of appearance, color, aroma, taste, texture, juiciness, tenderness, and acceptability (P>0.05). The compositional profile characteristics for chicks given compost at any level compared to chicks fed the control diet showed no differences (P>0.05). These findings suggest that the sensory characteristics and compositional profile of growing meat quails can be maintained when fed diets including up to 10% compost.

Assessing effect of feeding poultry byproducts compost on organoleptic characteristics and compositional profile of meat of broiler chickens.

Large amounts of waste, including dead birds, manure, and poultry litter, are produced by the poultry industry. Poultry waste should be disposed of properly to avoid major pollution and health risks. Composting litter and dead birds could be an option to recycle the waste and use in poultry feed. A study was conducted to investigate the effects of feeding composted poultry waste on the organoleptic qualities and compositional profile of the meat of broiler chickens. A total of 300 day-old broiler chicks (500-Cobb) were randomly allocated to five treatment groups replicated six times with 10 birds each, under a completely randomized design (CRD). Five iso-caloric and iso-nitrogenous diets including composted poultry byproducts at concentrations of 0, 2.5, 5, 7.5, and 10% were fed ad libitum to the birds from day 0 to day 35. The sensory grading and meat composition profile of 500 Cobb broiler chickens were tested at 35 days of age. The findings showed that there were no variations in the sensory profiles of the meat from birds given various diets (P>0.05). Although the results were somewhat lower for the chicks fed compost-containing diets than for the control group, this difference was deemed to be insignificant (P>0.05). Similarly, there were no variations in the compositional profile values of the meat between meat from birds fed various diets (P>0.05). These findings imply that broiler chickens may be raised on diets containing up to 10% poultry byproduct compost without any negative impacts on the meat's sensory quality or composition. Additionally, using compost into broiler diets may help to lower the cost of feed.

Effects of selenium supplementation on the growth performance, slaughter characteristics, and blood biochemistry of naked neck chicken.

This study examined how selenium-supplemented diets affected the performance of naked neck chickens. The birds were fed both organic and inorganic selenium at 0.30 ppm, while the control diet did not include any additional selenium. A total of 225 one-day-old naked neck chicks were randomly divided into 3 experimental groups, each of which was replicated 5 times (replicates) and contained 15 birds. This was done using a completely randomized design. The data was collected after growth, meat quality, and blood profile parameters were assessed. The findings showed that the birds fed inorganic selenium in the diet displayed increased (P < 0.05) feed intake followed by those administered organic selenium and the control diet. On the other hand, birds fed organic selenium in the diet showed enhanced body weight gain and better feed conversion ratio (P < 0.05). Similarly, organic selenium supplementation increased (P < 0.05) breast and thigh weight compared to inorganic selenium, but no other metrics, such as dressing percentage, drumstick weight, liver weight, gizzard weight, heart weight, or wing weight, significantly differed between treatments (P > 0.05). When compared to birds fed inorganic Se and control diet, the birds fed organic Se had greater (P < 0.05) blood levels of total protein and globulin. Additionally, it was discovered that organic Se-fed birds had greater (P < 0.05) blood Se concentrations than control and inorganic Se-fed birds. However, no differences between treatments were found in albumin, glucose, cholesterol, triglycerides, or uric acid (P > 0.05). In conclusion, adding Se-enriched yeast, as an organic selenium source, to diets may enhance the poor growth and slaughter characteristics of naked neck chicks without negatively affecting blood chemistry.

In-vivo nitrosation of amines in mice by inhaled nitrogen dioxide and inhibition of biosynthesis of N-nitrosamines.

Inhalation of nitrogen dioxide (NO2) by mice administered orally morpholine (MOR) or dimethylamine (DMA) resulted in the biosynthesis of N-nitrosomorpholine (NMOR) or N-nitrosodimethylamine (NDMA), respectively, as determined by the analysis of frozen whole-mouse powder, using gas chromatography with a Thermal Energy Analyzer detector. Significant levels of NMOR were detected following exposure of mice to 0.38 mg/m3 NO2 for 0.5 h (26 ng NMOR/mouse) and there was a two-fold increase when NO2 exposure was extended to 4 h. NMOR levels also increased in a time-dependent manner at 28.4 and 47.3 mg/m3 NO2 exposure levels, reaching a maximum of 450 and 725 ng NMOR/mouse, respectively, at 4 h. Oral administration of sodium ascorbate (50-250 mg), ammonium sulfamate (50-100 mg) or DL-alpha-tocopherol (67-167 mg) immediately after MOR or DMA, but prior to NO2 exposure, significantly inhibited both NMOR and NDMA biosynthesis, sulfamate being the most effective (greater than 90% NMOR and NDMA inhibition), followed by ascorbate (83-90% NMOR and 58-90% NDMA inhibition) and alpha-tocopherol (22-42% NMOR and 46-69% NDMA inhibition). Low levels of NDMA were found in untreated control mice (less than 13 ng/mouse) and in most samples of commercially obtained animal feed (10-15 micrograms/kg); NMOR, however, was not detectable or was detected in negligible amounts in these cases. Various control experiments indicated that most of the recovered nitrosamine resulted from in-vivo nitrosation in mice, with only up to 1-2% of NMOR and approximately 10% of NDMA yields being attributed to artefact formation, possibly during work-up of the mouse-powder samples.

DNA damage in isolated hamster and rat pancreas cells by pancreatic carcinogens.

N-Nitrosobis(2-oxopropyl)amine (BOP), N-nitrosobis(2-hydroxypropyl)-amine (BHP) and N-nitroso(2-hydroxypropyl-2-oxopropyl)amine (HPOP) are pancreatic carcinogens in the Syrian golden hamster (SGH) but do not cause pancreatic tumors in rats. In this study, the ability of these three compounds to induce DNA damage in isolated pancreas cells from both species was determined by alkaline elution analysis. BOP was highly potent in SGH cells, causing DNA damage at concentrations as low as 0.5 micrograms/ml, and HPOP, although less potent than BOP, also caused considerable damage. Isolated SGH pancreas cells are thus able to metabolize BOP and HPOP to DNA-damaging species. Of the three compounds tested, only HPOP at higher doses (25-100 micrograms/ml) induced DNA damage in isolated rat pancreas cells. BHP did not damage rat or SGH pancreas cell DNA at concentrations up to 100 micrograms/ml, apparently due to lack of uptake of this compound by the cells. The observed insensitivity to DNA damage in rat cells is consistent with the resistance of the rat pancreas to carcinogenesis by these three compounds. The sensitivity of SGH pancreas cells to BOP- and HPOP-induced DNA damage correlates with the high carcinogenicity of these compounds for the SGH pancreas.

Biosynthesis of dimethylnitrosamine in dimethylamine-treated mice after exposure to nitrogen dioxide.

These studies demonstrate the nitrosating potential of NO2 in vivo in ICR mice. Groups of mice were gavaged with 2 mg dimethylamine (DMA) and exposed to NO2 at levels from 0.04 to 44.5 ppm for periods up to 4 hours. Mice were individually frozen and blended to a powder, aliquots of which were homogenized in ice-cold dicholoromethane and 35% aqueous methanol. Concentrates of organic extracts were analyzed or dimethylnitrosamine (DMN) by a Thermal Energy Analyzer with a gas chromatograph interface. Biosynthesis of DMN was dose- and time-dependent with relation to NO2 exposure, reaching a maximum yield of 60-70 ng/mouse (0.0035% DMA conversion) at 2 hours. DMN biosynthesis was inhibited by sodium ascorbate and, more effectively, by ammonium sulfamate.

Role of nitrogen dioxide in the biosynthesis of nitraosamines in mice.

Groups of three to four mice were gavaged with aqueous solutions of 2 milligrams of morpholine, after which they were exposed to nitrogen dioxide in inhalation chambers at concentrations of 0.2 to 50 parts per million for up to 4 hours. At sequential intervals during the exposure, mice were frozen and pulverized in liquid nitrogen, and the mice powder was extracted with ice-cold 35 percent aqueous methanol and dichloromethane; organic-phase concentrates were analyzed for N-nitrosomorpholine with a thermal energy analyzer interfaced to a gas chromatograph. The N-nitrosomorpholine yields, ranging up to about 2.3 micrograms per mouse, were time-dependent relative to the duration of exposure to nitrogen dioxide and dose-dependent relative to the concentrations of nitrogen dioxide; control levels (in mice that were gavaged with morpholine or distilled water and then exposed to air instead of nitrogen dioxide) were less than 5 nanograms per mouse. These preliminary studies demonstrate the in vivo nitrosating potential of nitrogen oxides.

Kinetics of nitrosamine formation in mice following oral administration of trace-level precursors.

Groups of 3-5 Swiss CD1 mice were gavaged with aqueous solutions of sodium nitrite (250 micrograms), followed immediately by morpholine (5 micrograms) or dimethylamine (250 micrograms). At subsequent intervals, up to 30-60 min, mice were frozen, pulverized in liquid nitrogen and extracted with methylene chloride. Volatile nitrosamines were then quantitatively determined using a Thermal Energy Analyzer, interfaced to GC or HPLC. Biosynthesis of both N-nitrosodimethylamine (NDMA) and N-nitrosomorpholine (NMOR) showed a time-dependent increase for 3 and 9 min, respectively, followed by a steady decline. Levels of NDMA and NMOR were generally less than 0.1 ng/g in control mice gavaged with amine or nitrite alone. Zero-time recovery of NDMA and NMOR ranged from 50-70% and 70-90%, respectively. Biosynthesis of NDMA and NMOR was inhibited by prior administration of ascorbic acid, sodium ascorbate or ammonium sulfamate.

In vivo nitrosation of morpholine in mice by inhaled NO2.

Groups of 3-5 mice were gavaged with aqueous solutions of 2 mg morpholine and immediately exposed to 2-50 ppm levels of NO2 in inhalation chambers for periods of up to 3 hours. After exposure, mice were frozen and pulverized in liquid nitrogen, and aliquots of frozen powder (congruent to 8 g) were extracted with cold 35% aqueous methanol and methylene chloride. Concentrated methylene chloride solutions were analyzed for N-nitrosomorpholine (NMOR), using gas chromatography with a Thermal Energy analyzer detector. NMOR levels in controls (exposed to NO2 alone, or dosed with morpholine without subsequent NO2 exposure) were less than 5 ng/mouse. NMOR yields in test mice were time-dependent with respect to duration of NO2 exposure and dose-dependent with respect to NO2 levels. These preliminary studies demonstrate the in vivo nitrosating potential of nitrogen oxides.

Uptake and excretion of benzo[a]pyrene and its metabolites by the rat pancreas.

Following intravenous administration of [3H]benzo[a]pyrene ([3H]BP) to rats, uptake of radioactivity by the pancreas, per g of tissue, was approximately 16% of that of the liver. At 5 min following administration, unmetabolized BP in the pancreas, liver, and blood constituted 79, 50, and 49% of total BP uptake, respectively. The total uptake and unmetabolized BP in these tissues declined in a biphasic manner over the 2-hr observation period, during which only 0.03% of the total administered dose was excreted in pancreatic juice, as compared to 39% in bile; all radioactivity in pancreatic juice and bile was due to polar BP metabolites, including 3-hydroxy-BP. Pretreatment of rats with methylcholanthrene induced a significant increase in biliary, but not pancreatic, excretion of radioactivity. Administration of secretagogues caused a 2-fold increase in pancreatic, but not biliary, radioactivity.

Evidence of DNA repair in the guinea pig pancreas, in vivo and in vitro, following exposure to N-methyl-N-nitrosourethane.

The nature of DNA damage induced by N-methyl-N-nitrosourethane (NMUT) in the guinea pig pancreas, both in vitro and in vivo, and subsequent repair was investigated by alkaline sucrose density gradient analysis, using a non-radioactive fluorimetric procedure for DNA determination in gradient fractions. In vitro exposure of pancreatic slices to 20 mM NMUT for 30 min damaged DNA to less than 2.24 . 10(6) dalton fragments. However, incubation of NMUT-treated slices for 3 h in a fresh medium resulted in the repair of most of DNA damage, as indicated by the conversion of low molecular weight DNA fragments into heavy DNA of molecular weight comparable to DNA from control slices. Additionally, a single administration of NMUT (30 mg/kg, i.p.) to guinea pigs induced extensive DNA damage, to less than 2.24 . 10(6) dalton fragments in the pancreas within 4 h; similar DNA damage was observed in the liver. However, in the pancreas and liver of guinea pigs sacrificed at increasing intervals after NMUT administration, there was a gradual conversion of shortened DNA fragments to heavy high molecular weight DNA, indicating repair of DNA damage. It appears that most of DNA damage in the pancreas and liver was repaired by 14 and 7 days, respectively, following NMUT administration.

Hepatocarcinogenic effects of N-nitroso-N-methylurea in guinea pigs.

Intragastric administration of N-nitroso-N-methylurea to strain 13 male guinea pigs, at a weekly dosage of 7.5 mg/kg for 15 weeks and then twice weekly for a subsequent 15 weeks, induced high toxicity, as evidenced by weight loss and mortality and a high incidence of malignant neoplasms, over a total observational period of 40 weeks. The neoplasms included hepatic angiosarcomas, cholangiocarcinomas, and generalized lymphoblastic lymphomas.

Quantitation of dimethylnitrosamine in the whole mouse after biosynthesis in vivo from trace levels of precursors.

A simple and highly sensitive procedure is described for the recovery and quantitative identification of nanogram quantities of preformed N-nitroso compounds in the whole mouse. This procedure has also been applied to the quantitation of N-nitroso compounds after they have been biosynthesized from trace amounts of precursors. The whole animal is frozen in liquid nitrogen and homogenized to a frozen powder; the powder is then extracted and analyzed by a thermal energy analyzer interfaced to a gas-liquid and a high-pressure liquid chromatograph.

Metabolism of benzo(a)pyrene by guinea pig pancreatic microsomes.

The in vitro microsomal metabolism of the strain 13 guinea pig pancreas was investigated by determining the benzo(a)pyrene (BP) hydroxylase activity in the 9000 x g supernatant and microsomal pellet. BP hydroxylase activity in both 9000 x g supernatant and microsomal pellet of the pancreas was less than 1% of the activity in the respective liver fractions, However, pretreatment of animals with methylcholanthrene or BP at 20 mg/kg, for either 1 day or 3 consecutive days, markedly enhanced the BP hydroxylase activity of pancreatic microsomes over that of controls; the induction in the liver microsomes was less than 2-fold over that of controls. The hydroxylation of BP by pancreatic microsomes was linear with time over a 30-min period, with the rate of hydroxylation dependent on both the enzyme and substrate concentrations.

Effects of N-methyl-N-nitrosourethane on DNA synthesis in the guinea pig pancreas.

The effects of N-methyl-N-nitrosourethane (NMUT) on pancreatic DNA synthesis were investigated at sequential intervals following gavage of Hartley guinea pigs with a single dose of 30 mg/kg. There was a highly significant stimulation of DNA synthesis, as evidenced by increased incorporation of [3H] methyl-thymidine ([3H]TdR), throughout the whole pancreas and particularly in the duodenal segment, at 4 h following NMUT administration, thereafter, DNA synthesis declined sharply up to 24 h, and then recovered gradually to control levels from 24--96 h. DNA synthesis stimulated by NMUT was suppressed by hydroxyurea (HU), and hence is likely to represent replicative, rather than repair, synthesis.

Single-strand scission and repair of DNA in mammalian cells by bleomycin.

DNA single-strand breakage by bleomycin treatment of cultured mammalian cells was demonstrated by the method of alkaline elution. Elution patterns from treated L1210 cells indicated that part of the DNA was extensively broken while the remainder was affected to a lesser degree. This biphasic effect, which was less prominent in human fibroblasts, may reflect a selective sensitivity either of part of the cell population or of part of the DNA within individual cells. In both cell types, the DNA damage was at least partially repaired upon incubation of the cells after removal of drug. Bleomycin did not inhibit the rejoining of X-ray-induced single-strand breaks. The production and repair of DNA single-strand breaks after bleomycin treatment were the same in normal human and xeroderma pigmentosum fibroblasts, indicating that these events do not require the excision endonuclease that appears to be defective in these ultraviolet light-sensitive xeroderma cells.

Kinetics of DNA repair synthesis in guinea-pig pancreatic slices following in vitro exposure to N-methyl-N-nitrosourethane.

In vitro exposure of guinea-pig pancreatic slices to NMUT resulted in an increase in hydroxyurea-insensitive 3H-TdR incorporation into DNA; this represents DNA repair synthesis following NMUT-induced DNA damage. The kinetics of this hydroxyurea-insensitive 3H-TdR incorporation suggest that the NMUT-induced DNA damage is largely repaired within 2 hours.

Evidence of repair of DNA damage induced by 4-hydroxyaminoquinoline 1-oxide in guinea pig pancreatic slices in vitro.

In vitro exposure of guinea pig pancreatic slices to 4-hydroxyaminoquinoline 1-oxide (HAQO) resulted in increased [methyl-3H]thymidine ([3H]TdR) incorporation into DNA, both in the presence and absence of hydroxyurea (HU). Normal DNA replicative synthesis, but not DNA repair synthesis, was suppressed by HU. The increase in [3H]TdR incorporation into DNA damage induced by HAQO. Exposure of pancreatic slices to 10(-6) to 10(-5) M concentrations of HAQO did not significantly increase thymidine incorporation; however, a 15-min exposure to 10(-4) M HAQO induced a significant increase in HU-insensitive [3H]TdR incorporation into DNA. Kinetics of [3H]TdR incorporation suggests that most of the DNA repair synthesis occurs during the 2 hr following HAQO-induced DNA damage.