Studies of whole blood-associated acetaldehyde levels in teetotalers

We measured whole blood-associated acetaldehyde (WBAA) levels in 225 teetotalers (123 females, 102 males) between the ages of 18 and 86 years. Values were normally distributed, but mean values for females were significantly lower than for males (7.6 ± 0.6 vs. 7.9 ± 0.7 μM, p < 0.0001). There was a significant positive correlation with age for the entire group (r² = 0.149, p = 0.001) and for both sexes. The correlation with WBAA and age was stronger for females. Significant but lesser positive correlations were found between WBAA and other variables that increase with age, including glucose, fructosamine, cholesterol, alkaline phosphatase, serum glutamate pyruvate transaminase (SGPT), gamma glutamyl transpeptidase (GGT), and creatinine in the entire data set. Partial r analyses indicated that the correlations were mediated through the primary association of WBAA and age. We conclude that in individuals who do not consume ethanol there are significant sex differences in whole blood acetaldehyde and that the values increase throughout life.     

Sodium dehydroacetate levels in chicken tissues

Sodium dehydroacetate (Na-DHA), which has preservative and antimicrobial effects, is used as food and feed additive. However, there is little information on the Na-DHA levels in foods derived from animals fed Na-DHA. In this study, an HPLC-based method with methanol and 0.02% ammonium acetate (31:69, v/v) as the mobile phase was developed to determine Na-DHA residues in chicken muscle, liver, kidney, and skin fat tissues. Forty-eight yellow-plumage broiler chickens were administered 200 mg/kg Na-DHA in their feed for 30 d and sacrificed at different time points. In this study, the limit of detection was 0.08 mg/kg and the limit of quantification was 0.2 mg/kg. The residue concentration of Na-DHA in chicken tissues was <0.7 mg/kg. The elimination half-times of Na-DHA were 5.86 d for kidney tissues, 6.02 d for liver tissues, 8.88 d for muscle tissues, and 10.38 d for skin fat tissues. The residue levels of Na-DHA were lower than dehydroacetic acid in chicken tissues in our previous work, implying less risk of Na-DHA residue in chicken tissues compared to its acid.     

Isolation and cultivation of bovine ephemeral fever virus in chickens and chicken embryos.

Unadapted bovine ephemeral fever (BEF) virus was isolated from cattle blood after intravenous inoculation into chicken embryos. Infected embryos died or hatched as abnormal chickens. The chick embryo was slightly less sensitive to unadapted BEF virus than were Vero cell cultures, but the use of embryos avoids the several blind passages that are required to isolate BEF virus in unweaned mice. Chick embryos were considerably less efficient than Vero cell culture or unweaned mice in detecting Vero cell-adapted and mouse-adapted BEF virus respectively. Viraemia was demonstrated in chicken embryos at 1-4 days and in one-day-old chickens at 1-3 days after intravenous inoculation of BEF virus. BEF virus was demonstrated by isolation and by immunofluoresence in heart, brain, lung and liver of chicken embryos at 1-5 days and in lung and liver of one-day-old chickens at 1-2 days, after intravenous inoculation. The isolated viruses were confirmed as BEF virus by neutralization with immune mouse ascitic fluid. BEF neutralizing antibodies were produced in 4-week-old and adult chickens after intravenous inoculation with BEF virus.     

Uptake and tissue-specific distribution of selected polychlorinated biphenyls in developing chicken embryos

Fertilized chicken eggs were injected with high doses of individual polychlorinated biphenyl (PCB) congeners (0.5 microg of PCB 77, 9.8 microg of PCB 153, or 10.9 microg of PCB 180) before incubation to investigate the structure-specific uptake of these compounds by the embryo and their accumulation in brain and liver tissue. In accordance with earlier publications, a gradual uptake and accumulation of these compounds was observed during the last week of embryonic development. The PCB uptake and distribution to the specific tissues did not appear to be structure dependent. Wet-weight liver PCB concentrations (18, 266, and 278 ng/g at hatching for PCB 77, PCB 153, and PCB 180, respectively) were consistently two- to fourfold higher than carcass levels (7 ng/g of PCB 77, 117 ng/g of PCB 153, and 81 ng/g of PCB 180 at hatching). Whereas liver and carcass concentrations increased exponentially between day 13 of incubation and hatching, PCB levels in brain tissue remained unaltered (range, 0.6-1.0 ng/g of PCB 77 and 8-12 ng/g of PCB 153 and PCB 180 throughout the last week of incubation). Lipid analysis of the organs suggested that the lipid composition of brain may be an important factor explaining the low PCB accumulation in this tissue.     

Breath acetaldehyde following ethanol consumption.

Five pairs of volunteers were studied to determine the effect of drinking ethanol on breath acetaldehyde levels. On a given study day, samples of breath were obtained for measurement of acetaldehyde and ethanol from both participants at t = -1 h, t = -0.5 h, and at t = 0 to obtain baseline values. The drinkers were then given ethanol (0.3 g/kg body weight), and the controls given an equal volume of tap water. Breath samples were then taken at 0.5, 1, 1.5, 2 h, and hourly until t = 6 h. The last sample taken was at t = 23.5 h. Acetaldehyde levels in breath were quantified with a fluorigenic high-performance liquid chromatographic assay. Blood ethanol was approximated using a breath analyzer. Acetaldehyde in breath rose 50-fold at the 0.5-h, time point and returned to levels not significantly different from baseline values by 3-4 h. The mean peak blood ethanol values reached 0.055%. The t 1/2 elimination for ethanol was 1.6 h, and that for acetaldehyde was 2.25 h. Elimination of both acetaldehyde and ethanol in breath were initially 0 order. A significant correlation (r = 0.74) was found between baseline breath acetaldehyde levels and peak acetaldehyde levels. We conclude that acetaldehyde resulting from ethanol intake rapidly partitions into breath. The correlation of baseline breath acetaldehyde values with peak values found after an ethanol challenge indicate that measurement of breath acetaldehyde may be useful in the identification of individual differences in ethanol metabolism.     

Plasma thyroid hormones and corticosterone levels in blood of chicken embryos and post hatch chickens exposed during incubation to 1800 MHz electromagnetic field

Introduction

This study attempted to determine the effect of a 1800 MHz electromagnetic field (EMF) (only carrier frequency) on thyroxine (T₄), triiodothyronine (T₃) and corticosterone (CORT) concentrations in the blood plasma of chick embryos, and to investigate the effect of electromagnetic field (EMF) exposure during embryogenesis on the level of these hormones in birds that are ready for slaughter.

Material and Methods

Throughout the incubation period, embryos from the experimental group were exposed to a 1800 MHz EMF with power density of 0.1 W/m², 10 times during 24 h for 4 min. Blood samples were collected to determine T₄, T₃ and CORT concentrations on the 12th (E12) and 18th (E18) day of incubation, from newly hatched chicks (D1) and from birds ready for slaughter (D42).

Results

The experiment showed that T₄ and T₃ concentrations decreased markedly and CORT levels increased in the embryos and in the newly hatched chicks exposed to EMF during embryogenesis. However, no changes were found in the level of the analyzed hormones in the birds ready for slaughter. Differences in T₄ and T₃ plasma concentrations between the EMF-exposed group and the embryos incubated without additional EMF were the highest in the newly hatched chicks, which may be indicative of the cumulative effect of electromagnetic field on the hypothalamo-pituitary-thyroid axis (HPT).

Discussion

The obtained results suggest that additional 1800 MHz radio frequency electromagnetic field inhibits function of HPT axis, however, it stimulates hypothalamo-pituitary-adrenal axis by inducing adrenal steroidogenic cells to synthesize corticosterone. Further investigations are needed to elucidate the mechanisms by which radio EMFs affect HPT and HPA axis function in the chicken embryos.     

Sequential study of the pathology of Prudhoe Bay crude oil in chicken embryos

Ten microliters of Prudhoe Bay crude oil was applied to the shell of fertile leghorn chicken eggs on Day 9 of incubation. Gross and microscopic pathological changes were examined in embryos surviving 1, 2, 4, and 9 days after treatment. Liver necrosis, renal lesions, and extensive edema appeared 2 days after treatment and reached maximal prevalence 4 days after treatment. There was minimal repair of the lesions from Day 4 to Day 9 after treatment. Pathological changes, including liver necrosis, mineralization in the kidney, infiltration by a large number of heterophils in the liver and spleen, subcutaneous edema with formation of large blisters, and reduction in body weight and length were still present on Day 18 of incubation, close to hatching time.     

Effect of diet and disulfiram on acetaldehyde blood levels after ethanol in UChA and UChB rats

Acetaldehyde (AcH) levels in blood samples taken from different zones of the vascular system 2 h after a p.o. dose of ethanol (2.76 g/kg) were studied in UChA (low ethanol consumer) and UChB (high ethanol consumer) rats fed a diet devoid of animal products, diet 1 (D₁), and a diet containing fish meal, diet 2 (D₂), and in rats pretreated with disulfiram (600 mg/kg p.o.).The results showed that, while there is no significant difference between UChA and UChB rats fed D₁ with respect to blood AcH levels and the basal activity of the hepatic mitochondrial high-affinity aldehyde dehydrogenase (AlDH), a significant strain difference was observed in rats fed D₂, which induced high blood AcH levels in UChA rats but not in UChB ones. No strain differences were observed in blood ethanol levels in the two groups of rats.When rats fed D₁ were pretreated with disulfiram, the raising of AcH blood levels induced by ethanol after disulfiram was significantly higher in UChA than in UChB rats in suprahepatic vein, femoral vein, and tail blood. This difference was concomitant with a greater inhibition of the hepatic mitochondrial high-affinity AlDH activity in UChA rats than in UChB ones, whether disulfiram was administered in vivo or in vitro, which excluded the possibility that the strain difference would be caused by a different bioavailability of disulfiram.     

The effects of 2,4,5-trichlorophenoxyacetic acid and 2,3,7,8-tetrachlorodibenzo-P-dioxin on developing chicken embryos

Analytical grade 2,4,5-T and TCDD were dissolved in acetone and injected into the airspace of fertile chicken eggs. Toxicity studies suggest that the LD₅₀ for 2,4,5-T is 133.1 mg of 2,4,5-T per kg of egg weight. The LD₅₀ for TCDD was estimated to be 2.4 × 10^–4 mg of TCDD per kg of egg weight. A partitioned chi-square analysis of the embryo viability data and the nonparallel dose response lines obtained from 2,4,5-T and TCDD suggest an independent mode of action for the two chemicals.As a result of the injection of these two chemicals, increased liver weight to egg weight percentages occurred. Liver weight enlargement as a result of elevated nucleic acid content was ruled out based on the following observations: (1) both RNA and DNA levels per gram of liver tissue were depressed and (2) treatment group RNA to DNA ratios remained the same as controls.     

Embryotoxic effects of eight organic peroxides and hydrogen peroxide on three-day chicken embryos

Nine peroxides were tested for embryotoxicity in 3-day chicken embryos using the air-chamber method. The potencies were expressed by the ED50 for the total embryotoxic effect of the chemicals, including deaths and malformations, up to Day 14 of the incubation. The range of the ED50's was from 0.13 to 2.7 mumoles per egg and the order of the potencies was as follows: cyclohexanoneperoxide greater than cumolhydroperoxide greater than ethylmethylketoneperoxide greater than dibenzoylperoxide greater than acetylacetoneperoxide greater than perbenzoic acid-tert-butylester greater than dicumylperoxide greater than dilauroylperoxide greater than hydrogen peroxide. All nine peroxides caused malformations at a moderate frequency. The maximum percentage of malformed embryos of the treated varied from the 16% of perbenzoic acid-tert-butylester to the 56% of dicumylperoxide. The high percentage caused by the latter could, however, result from slow diffusion of high lethal doses from the air chamber to the embryo.     

Repeated exposure to acetaldehyde vapor. Studies in Syrian golden hamsters.

The subacute inhalation toxicity of acetaldehyde was examined with four groups of 20 hamsters each, exposed repeatedly to acetaldehyde vapor at concentrations of 0, 390, 1,340, and 4,560 ppm (six hr day, five days/week) for a 90-day period. The highest level induced growth retardation, ocular and nasal irritation, increased numbers of erythrocytes, increased weights of heart and kidneys, and severe histopathological changes in the respiratory tract that mainly consisted of necrosis, inflammatory changes, and hyper- and metaplasia of the epithelium. The upper segments of the respiratory tract were much more severely injured than the lower parts. At 1,340 ppm treatment-releated changes included increased kidney weights in males and slight hyper- and metaplastic changes of the tracheal epithelium; 390 ppm was considered a no toxic effect level.     

Deficient levels of dietary selenium suppress the antibody response in first and second generation mice

The effect of a selenium-deficient diet during prenatal and postnatal development on the immune response was investigated in the C57BL/6J mouse. When the selenium-deficient diet was administered postweaning, these was no effect on the serum chemistries, primary antibody response, or lymphoid organ weight. However, the secondary antibody response to a T-cell dependent antigen was diminished. Administration of the selenium-deficient diet during gestation, lactation, and postweaning development had no effect on the serum chemistry values or lymphoid organs. However, body weights and primary and secondary antibody responses were reduced. Similar results were obtained in both in vivo and in vitro assay systems.     

Dietary galacto-oligosaccharides mixture can suppress serum phenol and p-cresol levels in rats fed tyrosine diet

Phenols (phenol and p-cresol) are amino acid metabolites produced by intestinal bacteria. Some reports have demonstrated that the accumulation of phenols in the serum has toxic effects in renal failure patients. In this study, we found that phenols accumulated in the serum of rats given a tyrosine diet, and that dietary intake of a galacto-oligosaccharide mixture (GOS) suppressed the accumulation of phenols in serum. Rats were fed a basal diet, tyrosine diet (basal diet with 2.5% tyrosine) or GOS diet (tyrosine diet with 5% GOS) for 2 wk. The concentrations of phenols in the feces, cecal contents, serum and urine were determined. Concentrations of phenols in the serum, cecal contents and feces from rats fed the tyrosine diet were significantly higher than those in rats fed the basal diet. The concentrations of phenols in feces, cecal contents and serum, and urinary excretion in the GOS diet group were significantly lower than those in the tyrosine diet group. The pH of cecal contents was decreased by GOS intake. Furthermore, the serum concentrations of phenols were closely correlated with cecal concentrations. This finding suggested that concentrations of phenols in the serum reflected phenol production in the cecum contents. These results showed that dietary intake of GOS could modify the intestinal environment, and suppress the production of phenols in the intestinal tract and the accumulation of phenols in the serum. Thus, GOS may help improve the quality of life (QOL) of patients with renal failure.     

Short- and long-term effects of acetaldehyde on plasma.

The effect of low concentrations of acetaldehyde on activated partial thromboplastin time (APTT) and prothrombin time (PT) of Accuclot coagulation plasmas was monitored over a prolonged time to mimic effects observed in alcoholism. A prolongation of the APTT from 31.9 +/- 0.7 s to 32.6 +/- 0.9 s (n = 8; P =.007) was observed after a 30-min preincubation time with 140 microM acetaldehyde. However, a minimum of 3.6 mM acetaldehyde was required to extend the APTT from 36.6 +/- 1.0 s to 41.2 +/- 0.8 s (P =.001) over an 18-h exposure time. Plasma acetaldehyde levels as low as 2.24 mM caused elevation of PTs from 12.5 +/- 0.5 s to 14.4 +/- 0.2 s (P =.005) after a 24-h preincubation time. These findings seem to indicate that short-term contact of acetaldehyde with plasma, probably yielding reversible interactions, may interfere with APTTs to a greater extent than long-term contact, which would presumably yield stable, irreversible interactions. In comparing the effects of 8.94, 17.9, 89.4, and 447 mM acetaldehyde on the PTs of Level I, II, and III plasma, the PTs were most increasingly prolonged in Level III plasma and least prolonged in Level I plasma at each acetaldehyde concentration, although the plasmas have comparable protein concentrations. These findings seem to indicate that coagulation factors are sensitive to inactivation by acetaldehyde.     

GnRH antagonists suppress prolactin release in non-human primates.

GnRH antagonists, such as Antide, are being evaluated for potential contraceptive applications. Although their contraceptive efficacy clearly results from their rapid inhibitory effects on gonadotropin release, there remains the possibility of other incidental effects. Under certain physiological conditions, the release of prolactin (Prl) appears to be temporally related to the secretion of luteinizing hormone (LH) and hence by inference to the secretion of GnRH. Here, we examined the effects of the GnRH antagonist Antide on the release of LH and Prl. Under agonadal conditions, a remarkable concordance was seen between LH and Prl pulses with up to 100% of pulses being coincident. Administration of Antide resulted in a rapid parallel decline in both LH and Prl with LH levels falling by 50% within 2 h and Prl levels falling by 30-40%. At this dose of Antide (1.0 mg/kg, sc), pulsatile release of LH and Prl continued albeit at a much reduced amplitude. The administration of a bolus of exogenous GnRH in the face of GnRHant-induced suppression resulted in prompt release of LH and Prl in all 3 monkeys. Since Antide inhibits the release of LH and Prl in a parallel fashion, and GnRH re-stimulates the release of both hormones in a parallel fashion, we conclude that the synchronous pulsatile release of LH and Prl observed in the agonadal monkey is due to a direct action of GnRH. What this action is for Prl release, and how it relates to the control of dopamine or other neuroendocrine mechanisms normally controlling the release of Prl remains unclear. It also remains to be seen whether this GnRH antagonist-induced suppression of Prl will have physiologic significance.     

Attenuation mechanism of virulent infectious bronchitis virus strain with QX genotype by continuous passage in chicken embryos

The virulent isolate SDZB0808 of QX-type infectious bronchitis virus (IBV) was continuously passaged in chicken embryos for 110 generations. The safety and immune efficacy of the 110th generation of IBVs (P110) were evaluated. Damage was not found in the appearance of the 3-day-old specific-pathogen-free (SPF) chicks immunized with 10^4.5 EID₅₀ (median embryo infective dose) of P110 by intranasal and ocular administration. At 14 d after the vaccination with 10^4.5 EID₅₀ of P110, all the 3-day-old SPF chicks were immune from the attack of the homologous virulent strain SDZB0808 and the heterologous virulent strain SDIB821/2012. The whole genome sequencing of SDZB0808 of different generations (P1–P110) indicated that the replicase 1a sequences of P60–P110 all lost a length of 30 bp in the same region. Specific primers were designed according to the differences in the genomes of P1–P110. SYBR Green I real-time quantitative PCR was adopted to analyze the proportion of the viruses with 30 bp deletion in P60, P100, and P110. Results showed that with the passage in chicken embryos, the proportion of the viruses with 30 bp deletion gradually increased. Almost 100% of the viruses in the P110 had 30 bp deletion in the replicase 1a sequence. Therefore, the attenuation of IBV's virulence may be the outcome of directional screening in the chicken embryos. This work confirmed the high safety and immune efficacy of P110 in SPF chickens. Thus, P110 can serve as an attenuated IBV vaccine candidate.