Growth performance,antioxidant and immune status of Siberian sturgeon (Acipenser baeri) fed diets containing green tea extract and oxidized fish oil

The present study was conducted to determine the effects of dietary oxidized fish oil (OFO) and green tea extract (GTE) on growth performance, antioxidant status and immunological parameters in Siberian sturgeon (Acipenser baeri). Fish weighing about 108 g were randomly assigned to one of nine dietary treatments (control diet without OFO and GTE; diets containing only 25 or 50 mg/kg of GTE; diets containing 50 mg/kg of OFO combined with 0, 25 or 50 mg/kg of GTE; diets containing 100 mg/kg of OFO combined with 0, 25 or 50 mg/kg of GTE) with three replicates of 15 fish stocked in fiberglass tanks using a completely randomized design. Growth performance indices, immunological parameters and antioxidant status of all treatment groups were determined using appropriate assays and compared. Results showed that GTE could enhance growth performance. Feeding GTE alone or combined with the OFO could decrease the hepatosomatic index (HSI) and viscerosomatic index (VSI). Serum lysozyme activity and antibody level were increased significantly by GTE alone or combined with OFO compared to the oxidized diets (p < 0.05). Conversely, lipid peroxidation products and antioxidant enzyme activity were significantly lower in GTE treatment groups and those that received combination of GTE and OFO compared to the oxidized diets. Low‐density lipoprotein (LDL) level in GTE groups was lower than other treatment groups (p < 0.05) however, in OFO treatment groups the LDL level in fish serum was significantly increased in comparison with the other treatment groups (p < 0.05). GTE and OFO alone or combined together significantly decreased the levels of triglyceride and cholesterol compared to the control group (p < 0.05). In conclusion, immunological and biochemical parameters were improved by inclusion of GTE into Siberian sturgeon rancid diets which can protect fish from the oxidative damage challenged by dietary oil oxidation.     

Designing of a Novel Fusion Protein Vaccine Candidate Against Human Visceral Leishmaniasis (VL) Using Immunoinformatics and Structural Approaches

Leishmaniasis is caused by an obligate intracellular protozoan parasite. The clinical forms of leishmaniasis differ from cutaneous leishmaniasis, mucocutaneous leishmaniasis and visceral leishmaniasis (VL) which depend on the parasite species and the host’s immune responses. There are significant challenges to the available anti-leishmanial drug therapy, particularly in severe forms of disease, and the rise of drug resistance has made it more difficult. Currently, no licensed vaccines have been introduced to the market for the control and elimination of VL. A potential target for use in candidate vaccines against leishmaniasis has been shown to be leishmania Kinetoplastid membrane protein-11 (KMP-11) antigen. In this study, we chose KMP-11 antigen as target antigen in our vaccine construct. In addition, B-type flagellin (fliC) was used as an adjuvant for enhancing vaccine immunogenicity. The GSGSGSGSGSG linker was applied to link the KMP-11 antigen and fliC (KMP-11-fliC) to construct our fusion protein. Bioinformatics approaches such as; 3D homology modeling, CTL, B-cell, MHC class I and II epitopes prediction, allergenicity, antigenicity evaluations, molecular docking, fast simulations of flexibility of docked complex and in silico cloning were employed to analysis and evaluation of various properties of the designed fusion construct. Computational results showed that our engineered structure has the potential for proper stimulation of cellular and humoral immune responses against VL. Consequently, it could be proposed as a candidate vaccine against VL according to these data and after verifying the efficacy of the candidate vaccine through in vivo and in vitro immunological tests.

     

R620W functional polymorphism of protein tyrosine phosphatase non-receptor type 22 is not associated with pulmonary tuberculosis in Zahedan, southeast Iran

The protein tyrosine phosphatase non-receptor type 22 (PTPN22) gene, which encodes an intracellular lymphoid-specific phosphatase, is considered an important regulator of T-cell activation. We investigated a possible association between the PTPN22 C1858T (R620W) polymorphism and pulmonary tuberculosis in an Iranian population. Single nucleotide polymorphisms of PTPN22 C1858T (rs2476601) were genotyped in 172 pulmonary tuberculosis cases and 204 normal subjects from Zaheden, Iran. Frequencies of genotypes CC, CT and TT of the PTPN22 C1858T polymorphism were 98.3, 1.7 and 0% in the pulmonary tuberculosis patients, and 96.1, 3.9 and 0% in the control group, respectively (P = 0.239). The frequency of the minor (T) allele was 0.8% in pulmonary tuberculosis patients and 2.0% in controls. Significant differences were not observed in genotype or allele frequencies of PTPN22 C1858T in the comparison between pulmonary tuberculosis patients and healthy subjects in our Iranian population sample.     

Distribution and health risk assessment of heavy metals in soil surrounding a lead and zinc smelting plant in Zanjan,Iran

One of the problematic issues in soil pollution studies is heavy metal particles which are produced by mines and smelting units and spread through wind action and/or runoff. Pollution and health risk assessment of cadmium, lead, zinc, copper, and nickel in soil around the lead and zinc smelting factory was carried out in Zanjan City, Iran. Contamination factor (Cf), pollution load index (PLI), geoaccumulation index (Igeo), hazard quotient (HQ), hazard index (HI), and carcinogenic risk were pollution and human health risk assessment metrics in this study. Based on the Iranian soil guideline value, soil samples in the studied areas were contaminated the least by copper and nickel and the most by cadmium. PLI results showed that soils near the production line were heavily or extremely heavily polluted. The results of Cf and Igeo showed that lead and zinc were the most important contaminants. Health risk assessment indicated that lead and cadmium in soil were the main contaminants, which pose both carcinogenic and non-carcinogenic risks to human health; carcinogenic risk levels were unacceptably high (above 1 × 10^?4). It can be concluded that mining and smelting activities degrade soil quality in this region and the soil pollution might be extended to farming areas.     

Phenotypic characterization of a tobacco mutant impaired in auxin polar transport

A mutation in tobacco (Nicotiana tabacum L. cv `Xanthi') called lat (low auxin transport) that changes many morphogenic features throughout the life of the plant has been isolated. Abnormalities were observed in seed development, embryogenesis, cotyledon formation, leaf initiation and development, leaf veination pattern, and flower development. Selfed R₂ lat mutant plants set between 60% and 90% fewer seeds than wild-type tobacco, and about 10% of these seeds did not germinate. Non-germinating seeds contained either abnormal embryos or abnormal endosperm tissues. There was no uniformity in the stage at which embryonic development ceased in the aberrant seeds. Seedlings often revealed abnormal and highly varied phenotypes after germination. In some of these cases, cotyledons were heart-shaped, fused, cup-shaped, or cylindrical. Leaf morphology ranged from normal to cup-shaped, and some leaves occasionally produced shoots from the leaf midvein. Flowers ranged from normal to compound with occasional fused floral parts or split petals. Stamens were sometimes petal-like. This unusual assortment of phenotypic changes suggested that the mutation might affect a basic component of plant metabolism. We found that polar transport of indole-3-acetic acid (IAA) was reduced to about 9–19% of the wild-type level in the inflorescence axis of selfed R₂ lat mutants. In addition, supplementation of 1-naphthaleneacetic acid (NAA) to sterile media suppressed some of the abnormalities of the lat mutation so long as the plants grew there. Similarities in the phenotype of embryos, cotyledon and leaf shapes, translocation of labeled IAA, and response to applied NAA indicate that the lat locus of tobacco may be analogous to the pin locus of Arabidopsis, or produce a protein that functions in the same auxin-transport pathway. Received: 18 March 1997 / Revision received: 1 May 1997 / Accepted: 17 June 1997     

Permethrin-impregnated bednet effects on resting and feeding behaviour of lymphatic filariasis vector mosquitoes in Kenya

The impact of permethrin-impregnated bednets on resting and feeding behaviour of mosquito vectors of Wuchereria bancrofti, causing human lymphatic filariasis was studied in six pairs of villages (treated and untreated) before and after intervention. The study villages were in Kwale District, near the coast of Kenya, where Bancroftian filariasis is highly endemic, transmitted by a combination of both anopheline and culicine mosquito vectors. Mosquitoes were collected weekly in each village, indoors (using pyrethrum spray catches) and outdoors (using pit traps) during 3–4 months following the long rainy season. Of the filariasis vector species of mosquitoes collected in 1994 before intervention, 33.6% were members of the Anopheles gambiae complex, 30% were An. funestus and 36.4% were Culex quinquefasciatus. PCR analysis of the An. gambiae complex species collected in 1995 demonstrated that 98.5% were An. gambiae sensu stricto, 1% An. arabiensis and 0.5% An. merus. Introduction of impregnated bednets in 1995 significantly reduced the number of indoor-resting An. gambiae s.l. by 94.6% and An. funestus by 96.7%, but there was no change in the number of Cx quinquefasciatus collected indoors. The number of outdoor-resting An. gambiae s.l. was significantly reduced, whereas densities of An. funestus and Cx quinquefasciatus remained unaffected outdoors. ELISA analysis of mosquito bloodmeals showed a shift from human to animal feeding after the introduction of treated nets. The human blood index (HBI) for indoor resting Cx quinquefasciatus was reduced from 93.1% to 14.4%. Vector potential based on the HBI and mosquito density was estimated to be reduced by 99% for An. gambiae s.l., 98% for An. funestus and 97% for Cx quinquefasciatus and vectorial capacity would be suppressed even more by the impact on the vector survival rates (not measured). These results suggest that permethrin-impregnated bednets give effective personal protection against transmission of W. bancrofti by An. gambiae, An. funestus and Cx quinquefasciatus in East Africa.     

Water-soluble formulation of Coenzyme Q10 inhibits Bax-induced destabilization of mitochondria in mammalian cells

Oxidative stress leads to mitochondrial dysfunction, which triggers the opening of the permeability transition pores (PTP) and the release of pro-apoptotic factors causing apoptotic cell death. In a limited number of cell systems, anti-oxidants and free-radical scavengers have been shown to block this response. We have previously reported that coenzyme Q₁₀ (CoQ₁₀), an electron carrier in the mitochondrial respiratory chain, is involved in the reactive oxygen species (ROS) removal and prevention of oxidative stress-induced apoptosis in neuronal cells. However, the mechanism of this protection has not been fully elucidated. In the present study we investigated the effects of CoQ₁₀ on the mitochondrial events characteristic to apoptosis, especially on the function of pro-apoptotic protein Bax. Our results demonstrated that following a brief exposure of two human cell lines (fibroblasts and HEK293 cells) to H₂O₂ the intracellular levels of ROS and the association of Bax with the mitochondria significantly increased and the cells underwent apoptosis. Both of these events, as well as the release of cytochrome c from the mitochondria, were blocked by a 24 h pre-treatment with CoQ₁₀. It is therefore believed that CoQ₁₀ prevented the collapse of the mitochondrial membrane potential in response to the H₂O₂ treatment. Recombinant Bax protein alone caused the ROS generation and release of cytochrome c from isolated mitochondria and, again, CoQ₁₀ inhibited these Bax-induced mitochondrial dysfunctions.