Effect of dietary vitamin E on physicochemical and fatty acid stability of fresh and thawed lamb.

This study evaluated the effect of dietary vitamin E supplementation (1000mg of DL-α-tocopheryl acetate/kg of basal diet) on physicochemical and fatty acid stability of fresh and thawed lamb leg chops, frozen stored for 3, 6 and 9months. Legs were chopped, modified atmosphere packaged (70%O2/30%CO2) and maintained under retail conditions (4±0.5°C, with 14h fluorescent light) for 9days. Muscle α-tocopherol concentration was over 3.5-fold higher in supplemented samples than in control lambs. The effect of dietary vitamin E was independent of frozen storage, so these effects were analysed separately. Vitamin E supplementation reduced lipid oxidation (P≤0.001) and decreased metmyoglobin formation, leading to a more attractive colour of meat. Moreover, supplementation led to a higher percentage of polyunsaturated fatty acids. Therefore, vitamin E supplementation could be recommended for preserving either fresh or thawed lamb.

The combined effects of superchilling and packaging on the shelf life of lamb.

The aim of this study was to evaluate the effect of superchilled storage at -1° on the shelf life of lamb slices packaged in an O2 enriched (40% O2/30% CO2/30% Ar) or in an anaerobic atmosphere (vacuum skin packaging). Physicochemical, microbial and sensory analyses were performed. The effect of superchilled storage on lamb stability differed depending on the atmosphere surrounding the product. Superchilled (-1°C) slices of lamb showed lower microbial counts than those refrigerated at 4°C in both packaging conditions. Moreover, meat stored at -1°C had a higher colour stability under vacuum. Superchilled storage combined with an O2 enriched atmosphere increased the rate of lipid oxidation, which reduced the shelf life reached by refrigerating at 4°C. Vacuum skin packaging strongly inhibited lipid oxidation independently of storage temperature. Thus, superchilled storage extended the shelf life at least twice compared to storage at 4°C under anaerobic conditions while it was disadvantageous when an O2 enriched atmosphere was used.

Effect of borage and green tea aqueous extracts on the quality of lamb leg chops displayed under retail conditions.

Different concentrations of two aqueous extracts from green tea leaves and borage seeds with potential antioxidant activity were evaluated in lamb leg chops. Chops were sprayed with 0.005, 0.05, 0.5, 5% (p/v) green tea extracts (T) and 0.5, 5 and 10% (p/v) borage seed extracts (B) and displayed under retail conditions for 13days. Total polyphenols, TBARS, colour, microbial and sensory analyses were performed. The extracts showed a concentration-dependent action; the minimum concentration of polyphenols which significantly reduced lipid oxidation was 2.08mgGAE/100cm2 of meat. Both 0.5% T and 10% B limited colour deterioration, reducing also metmyoglobin formation. The extracts showed no antimicrobial effect, exceeding microbial counts of 7logCFU/cm2 at 13days of display. Sensory analyses determined that none of the extracts added herb odours or flavours to lamb. In conclusion, 0.5% T or 10% B extracts extended lamb shelf life from 8 to 11days, so both would be recommended for lamb chops preservation.

Characterization and isolation of immature neurons of the adult mouse piriform cortex.

Physiological studies indicate that the piriform or primary olfactory cortex of adult mammals exhibits a high degree of synaptic plasticity. Interestingly, a subpopulation of cells in the layer II of the adult piriform cortex expresses neurodevelopmental markers, such as the polysialylated form of neural cell adhesion molecule (PSA-NCAM) or doublecortin (DCX). This study analyzes the nature, origin, and potential function of these poorly understood cells in mice. As previously described in rats, most of the PSA-NCAM expressing cells in layer II could be morphologically classified as tangled cells and only a small proportion of larger cells could be considered semilunar-pyramidal transitional neurons. Most were also immunoreactive for DCX, confirming their immature nature. In agreement with this, detection of PSA-NCAM combined with that of different cell lineage-specific antigens revealed that most PSA-NCAM positive cells did not co-express markers of glial cells or mature neurons. Their time of origin was evaluated by birthdating experiments with halogenated nucleosides performed at different developmental stages and in adulthood. We found that virtually all cells in this paleocortical region, including PSA-NCAM-positive cells, are born during fetal development. In addition, proliferation analyses in adult mice revealed that very few cells were cycling in layer II of the piriform cortex and that none of them was PSA-NCAM-positive. Moreover, we have established conditions to isolate and culture these immature neurons in the adult piriform cortex layer II. We find that although they can survive under certain conditions, they do not proliferate in vitro either. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 76: 748-763, 2016.

Olfactory bulbectomy, but not odor conditioned aversion, induces the differentiation of immature neurons in the adult rat piriform cortex.

The piriform cortex layer II of young-adult rats presents a population of prenatally generated cells, which express immature neuronal markers, such as the polysialylated form of the neural cell adhesion molecule (PSA-NCAM) or doublecortin (DCX), and display structural characteristics of immature neurons. The number of PSA-NCAM/DCX expressing cells in this region decreases markedly as age progresses, suggesting that these cells differentiate or die. Since the piriform cortex receives a major input from the olfactory bulb and participates in olfactory information processing, it is possible that the immature neurons in layer II are affected by manipulations of the olfactory bulb or olfactory learning. It is not known whether these cells can be induced to differentiate and, if so, what would be their fate. In order to address these questions, we have performed unilateral olfactory bulbectomy (OBX) and an olfactory learning paradigm (taste-potentiated odor aversion, TPOA), in young-adult rats and have studied the expression of different mature and immature neuronal markers, as well as the presence of cell death. We have found that 14 h after OBX there was a dramatic decrease in the number of both PSA-NCAM and DCX expressing cells in piriform cortex layer II, whereas that of cells expressing NeuN, a mature neuronal marker, increased. By contrast, the number of cells expressing glutamate decarboxylase, isoform 67 (GAD67), a marker for interneurons, decreased slightly. Additionally, we have not found evidence of numbers of dying cells high enough to justify the disappearance of immature neurons. Analysis of animals subjected to TPOA revealed that this paradigm does not affect PSA-NCAM expressing cells. Our results strongly suggest that OBX can induce the maturation of immature neurons in the piriform cortex layer II and that these cells do not become interneurons. By contrast, these cells do not seem to play a crucial role in olfactory memory.

Interactions in developmental toxicology: effects of concurrent exposure to lead, organic mercury, and arsenic in pregnant mice.

The development toxicity of lead nitrate (25 mg/kg, SC), methylmercury chloride (12.5 mg/kg, PO), and sodium arsenite (6 mg/kg, SC) was assessed in CD1 mice following administration on gestation day 10 of these chemicals separately or in their binary and ternary combinations. Cesarean sections were performed on day 18 of gestation, and fetuses were examined for malformations and variations. Three fetuses from each dam were used for whole-body analyses of Pb, Hg, and As. Maternal toxic effects were more remarkable in the group concurrently exposed to Pb, Hg, and As than in those given binary combinations of the elements. In turn, maternal toxicity was more notable in these groups than in those given separately the test compounds. With regard to developmental toxicity, the most relevant effects (decreased fetal weight, cleft palate) corresponded to the Hg-treated groups. It is in agreement with the finding that in all experimental groups the levels of Pb and As in whole fetuses were under their respective detection limits. In general terms, the present data suggests that at the current doses, the interactive effects of Pb and As on Hg-induced developmental toxicity were not greater than additive. In contrast, exposure of pregnant mice to Pb and As at doses that were practically nontoxic to dams, concurrently with organic Hg at a toxic dose, caused supra-additive interactions in maternal toxicity.

Effects of oral aluminum on essential trace elements metabolism during pregnancy.

The present study was conducted to assess in rats the effects of oral aluminum (Al) exposure on calcium (Ca), magnesium (Mg), manganese (Mn), copper (Cu), zinc (Zn), and iron (Fe) accumulation and urinary excretion. Three groups of plug-positive Sprague-Dawley (SD) rats were given by gavage 0, 200, and 400 mg/kg/d of Al(OH)3 on gestational days 1-20. Three groups of nonpregnant female SD rats of the same age received Al(OH)3 by gavage at the same doses for 20 consecutive days. At the end of the treatment period, 24-h urine samples were collected for analysis of Al and essential elements. Subsequently, all animals were sacrificed and samples of liver, bone, spleen, kidneys, and brain were removed for metal analyses. With some exceptions, the urinary amounts of Al, Mn, and Cu excreted by pregnant animals as well as the urinary levels of Al excreted by nonpregnant rats were higher in the Al-treated groups than in the respective control groups. Although higher Al levels were found in the liver of pregnant rats, the concentrations of Al in the brain of these animals were lower than those found in the same tissues of nonpregnant rats. With regard to the essential elements, tissue accumulation was most affected in pregnant than in nonpregnant animals. In pregnant rats, the hepatic and renal concentrations of Ca, Mg, Mn, Cu, Zn, and Fe, as well as the levels of Ca in bone, and the concentrations of Cu in brain were significantly higher in the Al-exposed groups than in the control group. According to the current results, oral Al exposure during pregnancy can produce significant changes in the tissue distribution of a number of essential elements.

Nephrotoxicity of simultaneous exposure to mercury and uranium in comparison to individual effects of these metals in rats.

Both inorganic mercury and uranium are known nephrotoxicants in mammals. In this study, the renal toxicity of a concurrent exposure to inorganic mercury and uranium was compared with the nephrotoxic effects of the individual metals in a rat model. Eight groups of rats, 10 animals per group, were subcutaneously given a single administration of mercuric chloride (HgCl2, 0.34 mg/kg and 0.68 mg/kg), uranyl acetate dihydrate (UAD, 2.5 mg/kg and 5 mg/kg), or combinations of both compounds at the same doses. A ninth group of rats received sc injections of 0.9% saline and was designated as the control group. Necrosis of proximal tubules, which was observed in all experimental groups, was the most relevant morphologic abnormality. Marked changes, which were remarkably greater than those induced by the individual elements, were noted in some urinary parameters in the groups concurrently exposed to HgCl2 and UAD. It could be an indicator of a synergistic interaction between mercury and uranium. In contrast, compared with the urinary levels found after individual administration of the highest doses of mercury and uranium, significant reductions in the urinary concentrations of these elements were noted following simultaneous exposure to both metals. At these doses, the reduction in the urinary metal excretion was also accompanied by significant decreases in the renal content of mercury and uranium. Whereas the results of some parameters pointed out a possible synergistic interaction between mercury and uranium, other measures hinted that an antagonistic interaction between these elements is also present.

Evaluation of the protective activity of deferiprone, an aluminum chelator, on aluminum-induced developmental toxicity in mice.

BACKGROUND: Since deferiprone can be an effective chelating agent for the treatment of aluminum (Al) overload, in the present study we investigated whether this chelator could protect against Al-induced maternal and developmental toxicity in mice. METHODS: A single oral dose of Al nitrate nonahydrate (1,327 mg/kg) was given on gestation day 12, the most sensitive time for Al-induced maternal and developmental toxic effects in mice. At 2, 24, 48, and 72 hr thereafter, deferiprone was given by gavage at 0 and 24 mg/kg. Cesarean sections were performed on day 18 of gestation and fetuses were examined for malformations and variations. RESULTS: Aluminum-induced maternal toxicity was evidenced by significant reductions in body weight gain, corrected body weight change, and food consumption. Developmental toxicity was evidenced by a significant decrease in fetal weight per litter and an increase in the total number of fetuses and litters showing bone retardation. No beneficial effects of deferiprone on these adverse effects could be observed. By contrast, a more pronounced decrease in maternal weight gain and corrected body weight change, as well as a higher number of litters with fetuses showing skeletal variations was noted in the group exposed to Al nitrate and treated with deferiprone at 24 mg/kg. CONCLUSIONS: According to the current results, deferiprone would not be effective to prevent Al-induced maternal and embryo/fetal toxicity in mice.

Lack of protective effects of dietary silicon on aluminium-induced maternal and developmental toxicity in mice.

In recent years, it has been demonstrated that oral aluminium (Al) exposure can produce growth retardation, delayed ossification and an increased incidence of foetal abnormalities in rats and mice. On the other hand, it has been also suggested that silicon may have a protective effect in limiting oral Al absorption. The aim of the present study was to assess whether dietary silicon could prevent against Al-induced maternal and developmental toxicity in mice. On gestation days 6-15, Al nitrate nonahydrate (398 mg/kg/day) was given by gavage to three groups of pregnant animals, which also received silicon in drinking water at concentrations of 0, 118 and 236 mg/l on days 7-18 of gestation. Three additional groups of pregnant mice received respectively: 270.6 mg/kg of sodium nitrate (gavage), and silicon in drinking water at 118 and 236 mg/l. Although silicon administration at 236 mg/l significantly reduced the percentage of Al-induced deaths, abortions and early deliveries, neither 118 nor 236 mg/l of silicon produced significant ameliorations on Al-induced foetotoxicity. Under the current experimental conditions dietary silicon was not effective in protecting against Al-induced developmental toxicity.

Effects of simultaneous administration of desferrioxamine and tacrine in rats.

Tacrine (1,2,3,4-tetrahydro-9-aminoacridine), a reversible cholinesterase inhibitor, was effective in the treatment of Alzheimer's disease (AD). In turn, desferrioxamine (DFO), a chelating agent with ability to chelate iron and aluminum (Al), produced a 50% decrease in the rate of cognitive decline in patients with AD. Since combined therapy with tacrine and DFO might be more effective than individual administration of these drugs for the treatment of AD patients, this study evaluated the toxic effects of concomitant administration of tacrine and DFO to rats. Three groups of 8 rats each received the following treatments for 8 w: 80 mg DFO/kg/d i.m., 7.5 mg tacrine/kg/d po, or 80 mg DFO/kg/d i.m. +7.5 mg tacrine/kg/d po. A control group received distilled water by gavage daily and a 0.9% saline injection i.m. The administration of DFO + tacrine for 8 w did not increase most of the side effects caused by the individual DFO or tacrine administrations. These results open the possibility of considering the effectiveness of simultaneous administration of DFO and tacrine as a palliative treatment for AD patients.

Comparison of the effectiveness of 2,3-dimercaptopropanol (BAL) and meso-2,3-dimercaptosuccinic acid (DMSA) as protective agents against mercuric chloride-induced nephrotoxicity in rats.

The effectiveness of 2,3-dimercaptopropanol (BAL) and meso-2,3-dimercaptosuccinic acid (DMSA) on HgCl2-induced nephrotoxicity was studied in the rat. Seven groups of adult male rats were given a single sc toxic dose of HgCl2 (0.68 mg/kg) followed by 0.9% saline (positive control group), BAL (15, 30, and 60 mg/kg) or DMSA (50, 100, and 200 mg/kg) administered ip at 0, 24, 48, and 72 h thereafter. Although the renal function of HgCl2-exposed rats was slightly improved after BAL administration, Hg concentrations in the kidney were only reduced at 60 mg/kg. In addition, the protective effect of BAL was not dose-related. In contrast to BAL, DMSA was effective in increasing the urinary excretion of Hg and in reducing the renal Hg content. These results show that DMSA would be more effective than BAL in preventing or in protecting against inorganic Hg-induced nephrotoxicity.

Silicon reduces aluminum accumulation in rats: relevance to the aluminum hypothesis of Alzheimer disease.

In recent years, a possible relation between the aluminum and silicon levels in drinking water and the risk of Alzheimer disease (AD) has been established. It has been suggested that silicon may have a protective effect in limiting oral aluminum absorption. The present study was undertaken to examine the influence of supplementing silicon in the diet to prevent tissue aluminum retention in rats exposed to oral aluminum. Three groups of adult male rats were given by gavage 450 mg/kg/day of aluminum nitrate nonahydrate 5 days a week for 5 weeks. Concurrently, animals received silicon in the drinking water at 0 (positive control), 59, and 118 mg Si/L. A fourth group (-Al, - Si) was designated as a negative control group. At the end of the period of aluminum and silicon administration, urines were collected for 4 consecutive days, and the urinary aluminum levels were determined. The aluminum concentrations in the brain (various regions), liver, bone, spleen, and kidney were also measured. For all tissues, aluminum levels were significantly lower in the groups exposed to 59 and 118 mg Si/L than in the positive control group; significant reductions in the urinary aluminum levels of the same groups were also found. The current results corroborate that silicon effectively prevents gastrointestinal aluminum absorption, which may be of concern in protecting against the neurotoxic effects of aluminum.

Comparative effects of the chelators sodium 4,5-dihydroxybenzene-1,3-disulfonate (Tiron) and diethylenetriaminepentaacetic acid (DTPA) on acute uranium nephrotoxicity in rats.

Sodium 4,5-dihydroxybenzene-1,3-disulfonate (Tiron) and diethylenetriaminepentaacetic acid (DTPA) are two chelating agents that have been demonstrated to be effective in the treatment of experimental poisoning by a number of heavy metals. In this study, the effects of Tiron and DTPA on uranium-induced nephrotoxicity were evaluated in a rat model. A series of four Tiron or DTPA injections was administered intraperitoneally to adult male Sprague-Dawley rats immediately after a single subcutaneous injection of uranyl acetate dihydrate (5 mg/kg) and at 24, 48 and 72 h thereafter. Positive and negative control groups received 0.9% saline with or without uranyl acetate, respectively. Tiron effectiveness was assessed at 400, 800 and 1600 mg/kg, whereas DTPA was administered at 250, 500 and 1000 mg/kg. Although the urinary excretion of uranium was significantly enhanced by Tiron administration, significant amounts of uranium still remained in the kidney at the end of the treatment. However, the partial reduction of the renal uranium concentrations was in accordance with the amelioration noted in some urinary and serum indicators of uranium nephrotoxicity. Moreover, Tiron administration also reduced the severity of the uranium-induced histological alterations in the kidney. According to these results, Tiron offers only a modest encouragement with regard to its possible therapeutic potential to treat acute uranium-induced nephrotoxic effects. In turn, DTPA was less effective than Tiron in protecting against the nephrotoxicity of uranium in rats.

Impact of reduction of lead in gasoline on the blood and hair lead levels in the population of Tarragona Province, Spain, 1990-1995.

The limitation in the use of lead in Spanish gasoline has induced a resulting decrease in atmospheric lead concentrations, a remarkable reduction in the lead levels of edible vegetables, as well as a marked decrease in the dietary lead intake of the population of Tarragona Province (Catalonia, N.E. Spain). The present study evaluates the impact of such decreases on blood lead values and hair lead concentrations in an adult and children population of that region. A total of 250 adult participants between 16-65 years of age and 252 children were included in the study. Blood and hair samples were subjected to lead analyses by graphite furnace atomic absorption spectrophotometry and inductively coupled plasma spectrometry, respectively. A substantial decline in both, blood lead levels in adults (47.5%) and lead concentrations in children's hair (53%) was observed. During the period 1990-1995, blood levels were reduced from 12.0 micrograms dl-1 to 6.3 micrograms dl-1, while the hair lead concentrations decreased from 8.8 micrograms g-1 to 4.1 micrograms g-1. These decreases were noted for all the subgroups (sex, age and place of residence) examined, and were mainly attributable to the reduced leaded gasoline consumption.

Assessment of the protective activity of monisoamyl meso-2,3-dimercaptosuccinate against methylmercury-induced maternal and embryo/fetal toxicity in mice.

The protective activity of monoisoamyl meso-2,3-dimercaptosuccinate (Mi-ADMS), a new monoester of 2,3-dimercaptosuccinic acid (DMSA), on methylmercury-induced maternal and developmental toxicity was assessed in mice. A series of four Mi-ADMS injections was given s.c. at 0.25, 6, 24, and 48 h after oral administration of 25 mg/kg of methylmercury chloride (MMC) given on day 10 of gestation. Mi-ADMS effectiveness was tested at 0, 23.8, 47.6 and 95 mg/kg. Cesarean sections were performed on gestation day 18. All live fetuses were examined for external, internal, and skeletal abnormalities. Oral MMC administration resulted in an increase in the number of resorptions, and a decrease in fetal body weight, whereas the incidence of cleft palate, micrognathia, and skeletal variations was also increased in the fetuses of the MMC-treated groups. Although significant amelioration of MMC-induced embryolethality by Mi-ADMS was not noted at any dose, MMC-induced fetotoxicity was reduced by administration of this agent at 23.8, 47.6, and 95 mg/kg. However, the intrinsic toxicity of Mi-ADMS would be a restrictive factor for the possible therapeutic use of this chelator in pregnant women exposed to organic mercury.