Chicken Brain Tissue Research Articles

Neurotoxicity of xylazine in chicks

Despite the widespread use of xylazine in veterinary medicine, studies on its neurotoxicity are limited. So, our current study aims to reveal its neurotoxicity in chicks by determining the (LD50) of xylazine in Dixon's procedure. Moreover, it aims to study the effects of a small and repeated dose of xylazine on neurobehavioral test and the toxic doses of xylazine on the concentration of (glycine and glutamate) in the plasma of chicks and on the brain tissue after 60 and 90 minutes of injection. The LD50 of xylazine by injection into the chest muscle was 26.65 mg/kg. The injection of xylazine at a dose of 3 and 6 mg/kg in the chest muscle for three consecutive days caused an inhibition in motor activity within the open field as well as a significant elevation in the tonic immobility test response, injection of xylazine at doses 48.96 mg/kg ,60 and 90 minutes after the injection led to a significant increase in the glycine concentration as well as a significant decrease in glutamate after 90 minutes in the plasma of chicks, accompanied by histological variation in the brain tissue characterized by necrosis of neurons, vasogenic edema, neurophagia, cavities, infarction, necrosis of Purkinjean cell with decrees in the number of it. Our results revealed that xylazine had neurotoxic effects in chicks, represented by inhibition of neural behavior and motor activity within the open field, accompanied by a change in the concentration of glycine and glutamate in the plasma of chicks and histological variation in the brain tissue of chicks.

Neurobehavioral toxicity of copper sulfate accompanied by oxidative stress and histopathological alterations in chicks' brain

The aim is to investigate the sub-acute neurotoxic effects of copper sulfate in chicks on motor and neurobehavioral activity and its relation to oxidative stress and histopathological changes in chick brain tissue. Thirty chicks were employed in this experiment, randomly separated into 5 groups of 6 chicks. They were given the following concentration 2.5, 5, 10, and 15% of LD50. Each of the chicks is put through the following behavioral tests response to tonic immobility test, righting reflex, testing the motor activity of the chicks inside the open field box. Orally LD50 was 772 mg/kg, Recording an inhibition in the animal's movement in the open field and an increase in the chicks' dormancy duration. The effects are directly proportional to the increase in the chicks' dose. Copper sulfate in 2.5, 5, 10, and 15% of the LD50 showed a significant increase in malondialdehyde concentration, while 15% of LD50 recorded a significant decrease in glutathione and cholinesterase activity. All doses substantially decreased total antioxidant capacity in brain and liver tissue. Chick brain of copper sulfate 15% of LD50 shows in the cortex of cerebrum severe gliosis, satellitosis, perivascular and periaxonal edema, necrosis (karyorrhexis) of neuron, and apoptosis. The rest of the concentrations had histopathological alterations proportionate to the rise in the given dose. We concluded from this work that high concentrations of copper sulfate in the brain generated oxidative stress and histopathological alterations, which influenced chicks' neurobehavior and motor activity in the open environment.

Isolation and Cryopreservation of Toxoplasma gondii Isolates from Cats and Chickens from Selected Households in the Thika Region, Kenya

There is a shortage of information in Africa regarding the genotypic and phenotypic characteristics of the Toxoplasma gondii circulating in domestic cats (Felis catus) and the intermediate hosts such as chicken. The situation is compounded by a lack of collection of well-stored isolates. The present study was aimed at creating a cryobank of T. gondii bradyzoites, tachyzoites, and oocysts. The parasites were isolated from cats and chickens kept in households in the Thika region, Kenya. Eight (8) cat fecal samples positive for T. gondii oocysts and 38 chicken brain tissue cysts (bradyzoites) were obtained and used for propagation in mice before cryopreservation. For each sample from the cats, (two donors) BALB/c mice were infected orally with 1 x 104/ml of oocysts. From each chicken sample, (two donors) BALB/c mice were infected intraperitoneally with 20-30 tissue cysts. On the third day after infection, tachyzoites were harvested from the peritoneal cavity of one donor mouse. The other two infected mice were further monitored for eight weeks, euthanized and the brain tissue harvested for toxoplasma cysts which were purified and cryopreserved. From the mice infected with oocysts from the cats’ samples, 2 (25%) tachyzoites but a higher 8 (100%) isolation was obtained from brain tissue cysts. On the other hand, from chicken samples generated 18 (47.3%) tachyzoites and 38 (100%), tissue cysts were obtained. The isolated oocysts (from cats), tachyzoites, and tissue cysts (from mice) were cryopreserved using 15% glycerol as cryoprotectant and stored in liquid nitrogen (-196oC). After 6 months of cryopreservation, the viability of the isolates was tested using Trypan blue dye exclusion on a manual hemocytometer. Viability (99.5% - 96%) of the cryopreserved samples was maintained for the three toxoplasma stages and there was no significant change (p>0.05) in the viability of the parasites before and after cryopreservation. The cryobank will serve as a repository for subsequent studies on molecular and phenotypic characterization of T. gondii isolates from Kenya.

Chicken thalamic injury induced by copper (II) or / and arsenite exposure involves oxidative stress and inflammation-induced apoptosis.

Copper (Cu) is a toxic substance of heavy metals, and arsenic (As) is a toxic substance of metalloids. They all cause oxidative stress and have been widely studied in recent years. Studies have reported that Cu and As can cause inflammation in chicken brain tissue. To assess the toxicological effects of Cu and/or As chronic exposure on chicken thalamus, we used toxicologically relevant concentrations of Cu and As in the chicken diet for 12 weeks. By comparative analysis, we found that higher malondialdehyde (MDA), total antioxidant capacity (T-AOC), and proinflammatory mediator (NF-κB) were observed in the Cu and/or As co-exposed group, indicating that oxidation stress and inflammation are produced. In addition, we also observed mitochondrial kinetics and the generation of apoptosis. These include the gene and protein expression levels of Drp1, Opa1, Mfn1, Mfn2 and Bcl-2, Bax, p53. In conclusion, we believe that in the chronic poisoning of Cu and/or As, inflammation occurs in the chicken thalamus, causing oxidative stress and mitochondrial kinetics, which eventually leads to apoptosis.

Investigation of the effects of dichlorvos poisoning on AMPK signaling pathway in chicken brain tissues

Dichlorvos is a common crop insecticide widely used by people which causes extensive and serious environmental pollution. However, it has been shown that organophosphorus poisoning causes energy metabolism and neural disorders. The overall purpose of this study was to investigate the damage to brain tissue and the changes in AMPK signaling pathway-related gene expression after dichlorvos poisoning in chickens. White-feathered broiler chickens, as the research subjects of this experiment, were divided into three groups: control group, low-dose group (77.5% dichlorvos at 1.13 mg/kg dose) and high-dose group (77.5% dichlorvos at 10.2 mg/kg dose). Clinical symptoms were observed after modeling, and an integrative analysis was conducted using HE staining microscopy, immune-histochemical microscopy, electron microscopy and PCR arrays. The results showed that the high-dose group had more obvious dyspnea, salivation, convulsion and other neurological phenomena. Pathological sections showed that nuclear disintegration of neurons was most obvious in the low-dose group, and apoptosis of brain cells was most obvious in the high-dose group, and the mitochondrial structure was destroyed in the two poisoned group, i.e. low-dose group and high-dose group. PCR arrays showed that AMPK signaling pathway was inhibited and the expressions of genes involved in energy metabolism (ACACA and PRKAA1) were significantly changed. Furthermore, genes associated with protein synthesis (EIF4EBP1) were significantly upregulated. FASN and HMGCR expressions were significantly increased. There were significant changes in the expressions of cell cycle-related genes (STK11, TP53 and FOXO3). Organophosphate poisoning can cause a lot of nuclear disintegration of brain neurons, increases cell apoptosis, disrupts the energy metabolism of mitochondrial structure, and inhibits the AMPK signaling pathway. These results provide a certain idea and basis for studying the mechanism of AMPK signaling after organophosphorus poisoning and provide a research basis for the prevention and treatment of organophosphorus poisoning.

Arsenic affects inflammatory cytokine expression in Gallus gallus brain tissues

BackgroundThe heavy metal arsenic is widely distributed in nature and posses a serious threat to organism’s health. However, little is known about the arsenic-induced inflammatory response in the brain tissues of birds and the relationship and mechanism of the inflammatory response. The purpose of this study was to explore the effects of dietary arsenic on the expression of inflammatory cytokines in the brains of Gallus gallus.ResultsSeventy-two 1-day-old male Hy-line chickens were divided into a control group, a low arsenic trioxide (As2O3)-treated (7.5 mg/kg) group, a middle As2O3-treated (15 mg/kg) group, and a high As2O3-treated (30 mg/kg) group. Arsenic exposure caused obvious ultrastructural changes. The mRNA levels of the transcription factor nuclear factor-κB (NF-κB) and of pro-inflammatory cytokines, including inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), and prostaglandin E synthase (PTGEs), in chicken brain tissues (cerebrum, cerebellum, thalamus, brainstem and myelencephalon) on days 30, 60 and 90, respectively, were measured by real-time PCR. The protein expression of iNOS was detected by western blot. The results showed that after being treated with As2O3, the levels of inflammatory-related factor NF-κB and pro-inflammatory cytokines in chicken brain tissues increased (P < 0.05).ConclusionsArsenic exposure in the chickens triggered host defence and induced an inflammatory response by regulating the expression of inflammatory-related genes in the cerebrum, cerebellum, thalamus, brainstem and myelencephalon. These data form a foundation for further research on arsenic-induced neurotoxicity in Gallus gallus.

Neurotoxicity induced by arsenic in Gallus Gallus: Regulation of oxidative stress and heat shock protein response

Arsenic, a naturally occurring heavy metal pollutant, is one of the functioning risk factors for neurological toxicity in humans. However, little is known about the effects of arsenic on the nervous system of Gallus Gallus. To investigate whether arsenic induce neurotoxicity and influence the oxidative stress and heat shock proteins (Hsps) response in chickens, seventy-two 1-day-old male Hy-line chickens were treated with different doses of arsenic trioxide (As2O3). The histological changes, antioxidant enzyme activity, and the expressions of Hsps were detected. Results showed slightly histology changes were obvious in the brain tissues exposure to arsenic. The activities of Glutathione peroxidase (GSH-Px) and catalase (CAT) were decreased compared to the control, whereas the malondialdehyde (MDA) content was increased gradually along with increase in diet-arsenic. The mRNA levels of Hsps and protein expressions of Hsp60 and Hsp70 were up-regulated. These results suggested that sub-chronic exposure to arsenic induced neurotoxicity in chickens. Arsenic exposure disturbed the balance of oxidants and antioxidants. Increased heat shock response tried to protect chicken brain tissues from tissues damage caused by oxidative stress. The mechanisms of neurotoxicity induced by arsenic include oxidative stress and heat shock protein response in chicken brain tissues.

Application of the LUminometric Methylation Assay to ecological species: tissue quality requirements and a survey of DNA methylation levels in animals

The LUminometric Methylation Assay (LUMA) measures global DNA methylation. LUMA depends on digestion of DNA with methyl-sensitive and methyl-insensitive restriction enzymes, followed by pyrosequencing. Until recently, LUMA has been principally used for biomedical research. Here, we use chickens as a model to investigate sample quality issues relating to LUMA and then apply the method to ecological species. First, we assessed the effect of tissue storage conditions on DNA methylation values. This is an important consideration for ecological species because samples are not always ideally preserved and LUMA is sensitive to poor DNA quality. We found that good quality LUMA data could be obtained from chicken liver and brain tissues stored at 21°C for at least 2 and 12h, respectively. Longer storage times introduced nonspecific peaks to pyrograms which were associated with reduced DNA methylation. Repeatedly, freezing and thawing the tissues did not affect LUMA data. Second, we measured DNA methylation in 12 species representing five animal classes: amphibians (African and Western clawed frog), reptiles (green anole lizard), fish (yellow perch, goldfish, lake trout), mammals (American mink, polar bear, short-beaked common dolphin, Atlantic white-sided dolphin) and birds (chicken, Japanese quail). We saw a pattern of high DNA methylation in fish (84-87%), and intermediate levels in mammals (68-72%) and birds (52-71%). This pattern corresponds well with previous measures of DNA methylation generated by HPLC. Our data represent the first CpG methylation values to be reported in several species and provide a basis for studying patterns of epigenetic inheritance in an ecological context.

The effect of Se-deficient diet on gene expression of inflammatory cytokines in chicken brain

Selenium (Se) plays an important role in the brain development, function, and degeneration, nutritional encephalomalacia is closely related with dietary Se in avian. However, there is little evidence on the relationship between inflammation and encephalomalacia in avian and the mechanism which Se regulates the inflammatory response in brain tissues remains to be unclear. The present paper describes the effects of Se-deficient granulated diet on one transcription factor-nuclear factor kappaB and four pro-inflammatory cytokines-tumor necrosis factor, cyclooxygenase2, inducible nitric oxide synthase and Prostaglandin E synthase mRNA expression in the chicken brain tissues associated encephalomalacia. One hundred male chickens (1day old; Weiwei Co. Ltd., Harbin, China) were divided into two groups (50 chickens per group). The expression levels in the brain tissues (cerebral gray matter, cerebral white matter, marrowbrain, cerebellum, thalamus and brain stem) were determined by real-time PCR on days 15, 25, 35, 45, and 55, respectively. The results showed the productions of pro-inflammatory mediators were increased following Se-deficiency. These data indicate the correlations between nutritional encephalomalacia and inflammatory response and the activity of inflammatory response in chicken brain may be induced by Se-deficiency.

Chicken immunoregulatory Ig-like receptor families: An overview and expression details on ggTREM-A1

Paired immunoregulatory receptors facilitate the coordination of the immune response at the cellular level. In recent years, our group characterized chicken homologues to mammalian immunoregulatory Ig-like receptor families. The first part of this review focuses on the current progress on chicken immunoregulatory Ig-like receptor families. One of these receptors is gallus gallus TREM-A1, which was described as the only member of the chicken TREM family with activating potential. The second part of this review presents a study initiated to further characterize ggTREM-A1 expression. For this purpose we established real-time RT-PCR and generated a specific mab to analyze the expression profile of ggTREM-A1 on mRNA and protein level, respectively. GgTREM-A1 mRNA was predominantly expressed in macrophages, but was also detected in brain, bone marrow, bursa, thymus, spleen and PBMC. Analyzing ggTREM-A1 surface expression by mab staining validated the expression on macrophages. Additionally, we showed high expression on blood monocytes, heterophils and NK cells and on monocytes isolated from bone marrow. Moreover, we detected ggTREM-A1 protein also on thrombocytes, B and T cell subsets, but antigen expression seemed to be lower and more variable in these cells. Immunohistochemistry of chicken brain tissue, combining ggTREM-A1 mab and various markers specific for various brain cell subsets showed expression of ggTREM-A1 on microglial cells, but also on neurons, astrocytes and oligodendrocytes. In conclusion, ggTREM-A1 is expressed on a variety of cells, relevant for the immune system, possibly combining physiological function of different mammalian TREM.

Computational Systems Biology

Computational Systems Biology

Attenuated L1 expression by glioma cells results in decreased cell migration on monolayer co‐cultures

L1 is a neural recognition molecule primarily responsible for the invasive quality of glioblastoma multiforme (GBM) cells. It acts by signaling through integrin receptors, and more recently discovered, the fibroblast growth receptor (FGFR). In addition, L1 is abnormally expressed, proteolyzed by ADAM10, and released (shed) by high‐grade glioma cell lines. Using short‐hairpin RNA (shRNA) and recombinant DNA techniques, we used lentiviral vector to shut down L1 expression in a L1 expressing glioma cell line (T98G). The effect of attenuated L1 expression by glioma cells on cell motility was measured on a substratum of axons and glial cell monolayer isolated from embryonic chick brain tissue. The results show that glioma cells that secrete L1 (T98G‐pLKO.1) display greater motility on monolayer co‐cultures than glioma cells that do not secrete L1 (T98G‐shL1). Research support was provided by Howard Hughes Medical Insititute.

Cellular transcripts of chicken brain tissues in response to H5N1 and Newcastle disease virus infection

BackgroundHighly-pathogenic avian influenza (HPAI) H5N1 and Newcastle disease (ND) viruses are the two most important poultry viruses in the world, with the ability to cause classic central nervous system dysfunction in poultry and migratory birds. To elucidate the mechanisms of neurovirulence caused by these viruses, a preliminary study was design to analyze host's cellular responses during infections of these viruses.MethodsAn improved mRNA differential display technique (Gene Fishing™) was undertaken to analyze differentially expressed transcripts regulated during HPAI H5N1 and velogenic neurotropic NDV infections of whole brain of chickens. The identification of differentially expressed genes (DEGs) was made possible as this technique uses annealing control primers that generate reproducible, authentic and long PCR products that are detectable on agarose gels.ResultsTwenty-three genes were identified to be significantly regulated during infections with both viruses, where ten of the genes have been selected for validation using a TaqMan® based real time quantitative PCR assay. Some of the identified genes demonstrated to be key factors involving the cytoskeletal system, neural signal transduction and protein folding during stress. Interestingly, Septin 5, one of the genes isolated from HPAI H5N1-infected brain tissues has been reported to participate in the pathogenic process of Parkinson's disease.ConclusionsIn this limited study, the differentially expressed genes of infected brain tissues regulated by the viruses were found not to be identical, thus suggesting that their neurovirulence and neuropathogenesis may not share similar mechanisms and pathways.

Characterization of the chicken galanin type I receptor (GalR1) and a novel GalR1-like receptor (GalR1-L)

Galanin is a multi-functional neuropeptide that is widely distributed in the mammalian central nervous system and peripheral tissues. It exerts multiple physiological functions through interaction with 3 known G protein-coupled receptors (GPCR), namely, galanin type I, II and III (GalR1, 2 and 3) receptors, which have only been identified in mammals. In this study, we reported the cloning and characterization of chicken galanin type I receptor (GalR1) and a novel galanin receptor with considerable homology to chicken GalR1, which herein is designated as galanin type I-like receptor (GalR1-L). Chicken GalR1 and GalR1-L full-length cDNAs were cloned from chicken brain and small intestine tissue, respectively. The former encodes a protein of 357 amino acids that shares 84–86% amino acid sequence identities with its mammalian counterparts, whereas the latter encodes a 363-amino acid protein with comparatively lower identities (55–56%) to the mammalian GalR1. Using reverse transcription (RT)-PCR assays, we examined the expression of both receptors in adult chicken tissues. Both receptors were found to be widely distributed in the tissues examined, including brain, small intestine, kidney, ovary, pancreas, pituitary and spleen. Interestingly, cGalR1 expression was detected in different regions of chicken oviduct, while cGalR1-L expression was restricted to the vagina. Using a pGL3-CRE luciferase reporter system, chicken galanin peptide (1–29) was demonstrated to inhibit both basal and forskolin-stimulated luciferase activities, in dose-dependent manners, through the cAMP-mediated signaling pathway in Chinese hamster ovary (CHO) cells expressing either cGalR1 or cGalR1-L, thus suggesting the functional couplings of both receptors to G i proteins. Together, the characterization of chicken GalR1 and GalR1-L provides a better understanding of the physiological roles of galanin in avian species.

Proteomics Analysis of Differential Expression of Chicken Brain Tissue Proteins in Response to the Neurovirulent H5N1 Avian Influenza Virus Infection

A certain H5N1 avian influenza virus has gained the ability to cause the classic central nervous system dysfunction in poultry and migratory birds. This study presents the proteomics analysis on the change of proteins to H5N1 avian influenza virus with neurovirulence infection in chicken brain tissue. By using 2-DE, coupled with MALDI-TOF MS/MS, we identified a set of differentially expressed cellular proteins, including 18 up-regulated proteins and 13 down-regulated proteins. The most significant changes were found in cytoskeleton proteins, proteins associated with the ubiquitin-proteasome pathway, and neural signal transduction proteins. Some identified proteins such as CRMP and SEP5 were found to participate in the pathogenesis progress of Parkinson's and Huntington's diseases, which also developed encephalitis accompanied with CNS dysfunction. The obtained data can provide insight into the virus-chicken brain tissue interaction and reveal the potential mechanism of the neuropathogenesis when the host was infected by the neurovirulent avian influenza virus.

A novel prolactin-like protein (PRL-L) gene in chickens and zebrafish: Cloning and characterization of its tissue expression

In this study, a full-length cDNA encoding a prolactin-like protein (PRL-L) was cloned from chicken brain tissues using RT-PCR. This putative PRL-L precursor has 225 amino acids in length and shares 30–35% amino acid sequence identity with prolactin (PRL) of chicken, zebrafish, Xenopus, rat and human. Using RT-PCR, the mRNA expression of PRL-L in chicken tissues was further examined. Unlike the predominant expression of PRL in pituitary, PRL-L was found to be widely expressed in adult chicken extra-pituitary tissues with only minimal expression detected in pituitary. In day-7 chicken embryos, the expression of PRL-L, but not PRL, was also detected in all extra-pituitary tissues examined. In line with this finding, the 5′-flanking region of chicken PRL-L (cPRL-L) gene, but not PRL gene, displayed a strong promoter activity in cultured DF-1 cell (a chicken embryo fibroblast cell line), suggesting that the basal expression of PRL-L gene is controlled by a transcriptional regulatory mechanism different from that of PRL gene. As the same findings in chickens, PRL-like protein(s), which share high amino acid sequence (42–86%) identity with chicken PRL-L, was identified in several non-mammalian vertebrate species including zebra finch, tiger puffer, green puffer and zebrafish. RT-PCR assay demonstrated that zebrafish PRL-L, similar to chicken PRL-L, is expressed in extra-pituitary tissues including brain, gill, muscle, ovary and testis. Taken together, these findings strongly suggest that a novel PRL-like protein exists in some non-mammalian vertebrates and may play an important role in target tissues, such as extra-pituitary tissues of chickens and zebrafish.

Functional autoradiography and gene expression analysis applied to the characterization of the α 2-adrenergic system in the chicken brain

Here we report a functional autoradiographic study of [ 35S]GTPγS binding induced by α 2-adrenoceptor activation in chicken brain tissue sections using both 10 −4 M UK 14304 (bromoxidine or brimonidine) and 10 −6 M epinephrine as α 2-adrenoceptor agonists. Assays were performed using two different incubation buffers: glycylglycine or Tris–HCl. Changes in the [ 35S]GTPγS basal binding values were detected, and different [ 35S]GTPγS specific binding values were also obtained depending on the buffer used for each drug. The best results were obtained with epinephrine in Tris–HCl, with slightly higher stimulation values than the observed with UK 14304 in glycylglycine buffer. The effect of the addition of adenosine deaminase to the incubation buffer was also tested. This effect decreasing basal binding in chicken was very small when compared to mammals, according with differences found in adenosine 1 receptor expression levels. Structures presenting α 2-adrenoceptor-mediated G i/o protein stimulation fitted with areas previously described as enriched in α 2-adrenoceptors in chicken brain, and their homologous areas in mammals. These data confirm the specificity of the results and reinforce the implication of the α 2-adrenoceptors in the function of these brain nuclei. On the other hand, the expression level of the different α 2-adrenoceptor subtypes was tested with real-time PCR. Contrasting with the α 2-adrenoceptor subtype distribution previously described with radioligand competition assays, where α 2A was the predominant α 2-adrenoceptor subtype (≥75%); in the present work, the ratio of α 2A:α 2B/C gene expression was lower than expected both in telencephalon, tectum opticum, and cerebellum.

13-P027 Injection of acidic fibroblast growth factor (FGF-1) into the cisterna magnum induces Glypican-1 expression in the chick brain tissue

13-P027 Injection of acidic fibroblast growth factor (FGF-1) into the cisterna magnum induces Glypican-1 expression in the chick brain tissue

Induction of metallothionein in chick embryos as a mechanism of tolerance to platinum group metal exposure

Recent data show that platinum group metals (PGMs), primarily platinum (Pt), palladium (Pd) and rhodium (Rd), from automobile catalytic converters are being deposited in the environment. We investigated the PGM neurotoxicity and tolerance mechanism by induction of metallothionein (MT) in developing chick embryos. Chick embryos were injected on the 7th and 14th days of incubation with different concentrations of Pt and mixture of Pt, Pd and Rh (PGM mix) solutions. It is documented that induction of MT by zinc (Zn+2) protects against metal and non-metal hepatotoxicity. In this study the MT induction was examined through pretreatment of the two highest Pt(IV) exposure levels with exogenous Zn2+ on the 4th and 11th days of incubation. SDS-PAGE assay and digital image system were used to identify and quantify MT in homogenized brain and liver tissues. Quantitative analysis revealed an increase of MT in the 5 ppm Pt exposure as compared to controls. The 10 ppm Pt treatment was a lethal dose for exposed embryos. There was increased mortality at the 1.0 PGM mix level. The interaction of Pt, Pd and Rh in the mixture seems to favor metal accumulation and MT induction in the liver but not the brain. Pretreatment with exogenous Zn2+ increased chick survival. These results indicate that induction of MT plays a protective role against PGM toxicity. Metal analysis using atomic absorption spectrometer in graphite furnace mode (GFAAS) revealed PGM accumulation in chick embryo liver and brain tissues proportional to exposure concentration. Our results may imply that MT has an important role as a tolerance mechanism against PGM toxicity. The presence of Pt(IV) in brain tissue suggests that the undeveloped blood-brain barrier is permeable to PGMs. This raises concerns regarding the implication of these metals on neural injury.

The effect of dietary supplementation with blueberry, α-tocopherol or astaxanthin on oxidative stability of Arctic char ( Salvelinus alpinus) semen

The objective was to determine the oxidative stability of Arctic char ( Salvelinus alpinus) semen following dietary supplementation with lowbush blueberry ( Vaccinium angustifolium) product, α-tocopherol, α-tocopherol + blueberry product, or α-tocopherol + astaxanthin. Sperm lipid peroxidation was initiated by challenging with ferrous sulphate/ascorbic acid (Fe ++/Asc) at level of 0.04/0.2 mmol/L. Addition of blueberry, α-tocopherol, or both to char diets inhibited semen lipid peroxidation by: (a) decreasing the rate of sperm lipid peroxidation, an effect which was more pronounced with α-tocopherol treatments; and (b) increasing the antioxidant potential of seminal plasma, based on the lipid peroxidation process of sperm and an in vitro chicken brain tissue model. Dietary supplementation with astaxanthin and α-tocopherol had the same effect as the supplementation with α-tocopherol alone on inhibiting the lipid peroxidation process of sperm and chicken brain. Catalase-like activity increased significantly in sperm of fish fed α-tocopherol, blueberry, or both. There was a negative correlation ( r = −0.397, P < 0.05) between catalase-like activity in sperm cells and the rate of sperm lipid peroxidation. Seminal plasma α-tocopherol levels increased significantly in fish supplemented with α-tocopherol alone or in combination with blueberry or astaxanthin. There were negative correlations between seminal plasma α-tocopherol levels and lipid peroxidation rates of sperm cells ( r = −0.625, P < 0.01) and brain tissue ( r = −0.606, P < 0.01). In conclusion, dietary supplementation of blueberry product or α-tocopherol inhibited lipid peroxidation in Arctic char semen. Further experiments are needed to test the effect of dietary blueberry and antioxidants on Arctic char semen quality during liquid and cryopreserved storage.