[Effects of Ni2+ on physiological characteristics and submicroscopic structure of Salvinia natans leaves].

Influence of 0, 5, 10, 15, 20 mg/L Ni2+ on growth, mineral nutrition, chlorophyll, carotenoid, soluble protein, soluble sugar, superoxide (O2*-), hydrogen peroxide (H2O2) and malondialdehyde (MDA) contents as well as the activities of superoxide dismutase (SOD), guaiacolperoxidase (POD), and catalase (CAT) were studied in the leaves of Salvinia natans plants on 10 days after treatment. With the increase of the Ni2+ concentrations, exposure of the plants revealed that, (1) the addition of Ni2+ affected the absorption of mineral nutrients, it mainly increased the absorption of Ca2+, Na+, Zn2+, Fe3+ and Mg2+, while reduced that of Mn2+, Mo2+, P and K+. (2) The content of chlorophyll, carotenoid, soluble protein and soluble sugar content as well as activities of SOD and CAT decreased gradually. That of O2*-, H2O2 and MDA content as well as POD activity increased, 383%, 168%, 207%, 131% of these controls, respectively. (3) In the leaves of Ni2+ -treated fronds, the polypeptide with apparent molecular weights 94000, was became visible in SDS-PAGE, and the nature of it remains to be determined. The amount and intensity of polypeptide band increased gradually with augment of Ni2+ was also observed, the polypeptide with apparent molecular weight 35,000 increased significantly in fronds. (4) Transmission electron microscope observation indicated that Ni2+ also imposed injury action on submicroscopic structure of leaf cells, disaggregation of nucleolus, agglutination and disappearance of chromatin of nucleus, disruption of nuclear membrane, swelling of thylakoids and breakage of chloroplast envelope, decreasing of cristae quantity and vacuolization of mitochondria. The conclusion could be reached that the plant death was resulted from destruction under structure foundation of physiological function, unbalance of ion equilibrium and disorder of physiological metabolism.

[Toxic effects of Hg2+, Cd2+ and Cu2+ on cell membrane system of Cabomba caroliniana A. Gray].

By the observation with electron- and confocal laser scanning microscopy and the determination of physiological and biochemical reactions, the toxic effects of Hg2+, Cd2+ and Cu2+ on the cell membrane system of Cabomba caroliniana A. Gray were investigated. The results showed that under the actions of the three heavy metal ions, the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) in C. caroliniana leaf cells increased, activities of protective enzymes were in disorder, and lipid peroxidation happened. The cell membrane was damaged, membrane permeability increased, and plasmolysis occurred. Meanwhile, the chloroplast swelled or even disintegrated. The excitement of photosynthetic pigments on thylakoids membrane by light was inhibited, and the auto-fluoresent intensity was decreased. The cristae of mitochondria swelled and decreased, mitochondria membrane was damaged, and nuclear membrane was broken. The effects of Hg2+, Cd2+ and Cu2+ on the cell membrane system of C. caroliniana showed a definite dose-effect correlation, and the stability of membrane system played a key role in the resistance of C. caroliniana to the toxic effects of heavy metals. C. caroliniana was sensitive to Hg2+, and the lethal concentration of Hg2+ was ranged from 0.3 to 0.5 mg L(-1). C. caroliniana had relatively higher endurance to Cd2+ and Cu2+, and could be used as the resistant plant for biological control.

Early-phase endotoxic shock-induced myocardial injury increases iNOS and selectin expression in macaque primate.

BACKGROUND: Our previous study has established a macaque model with early-phase endotoxic shock. The present study further investigated myocardial and blood vessel injury in Macaques by examining the subsequent expression of ACP, selectins, iNOS, and cTnI in response to LPS treatment. METHODS: In an experiment with anaesthetised, instrumental macaques, eleven animals were randomised into: an En group (n=6), receiving a dose of 2.8 mg kg(-1) lipopolysaccharides (LPS) by i.v.; and a Co group (n=5), injected with normal saline of 1 ml kg(-1). Cytochemistry of acid phosphatase (ACPase) in heart was performed by electron microscope at 120 min following endotoxin injection. Three immunochemical stains, namely, L-selectin, P-selectin and iNOS protein in heart, were studied. In addition, cardiac troponin I (cTnI), L-selectin and P-selectin in plasma were detected. RESULTS: In the early phase of endotoxic shock, LPS caused myocardial lysosome damage. The data of immunochemical staining showed the thrombus formation in vessels and the increase of iNOS, L-Selectin and P-Selectin expression in heart, but LPS challenge did not change L-selectin, P-selectin and cTnI in plasma. CONCLUSION: The increase of iNOS, L-selectin and P-selectin protein expression following endotoxin administration may have caused vessel injury and myocardial damage in macaques.

Bovine immune colostrum against 17 strains of diarrhea bacteria and in vitro and in vivo effects of its specific IgG.

Bovine colostral antibodies of cows immunized with a multivalent vaccine consisting of whole cells of 17 strains of pathogenic diarrhea bacteria were generated, and the specific IgG with high activities and titres directed against these pathogens was purified using an ammonium sulfate precipitation and verified by SDS-PAGE. We demonstrate that specific IgG has a strong activity of inhibiting in vitro growth and colonization in pathogens by agglutinating with bacteria and destroying cell walls. Normal IgG purified from non-immunized bovine colostrum is incapable of eliciting the same consequences as specific IgG. Specific IgG prevents enteroinvasive Escherichia coli/Salmonella typhi-induced diarrhea and may exert an effective protection by enhancing splenic NK cell activity, elevating IL-2 level and inhibiting excessive release of TNF-alpha in mice. Thus, the specific IgG from colostral antibodies of immunized bovine can provide effective protection or therapy for multibacteria-induced diarrhea.

Endotoxic shock model with fluid resuscitation in Macaca mulatta.

These studies established a macaque model of early-phase endotoxic shock, and investigated the resuscitation effects of three different solutions. Twenty-four macaques were assigned to four groups. Nineteen animals were given an intravenous dose of 2.8 mg/kg lipopolysaccharide (LPS). At 60 min after LPS challenge, the animals were given (i) 5 mL/kg normal saline (Ns group, n=6), (ii) 5% of 5 mL/kg sodium bicarbonate (Sb group, n=6), (iii) hypertonic 3.5% sodium chloride of 5 mL/kg (Hs group, n=7). The control group (Co group, n=5) was first injected with 1 mL/kg Ns and with 5 mL/kg Ns 60 min later. Haemodynamic parameters and blood gases were measured during the experiment, and myocardial morphology was examined on termination of the experiment. Administration of LPS caused hypotension and decreases of the left ventricular work index (LVWI). In the Sb group, mean arterial pressure, cardiac index, systemic vascular resistance index, LVWI and right ventricular work index were significantly higher than those of the Ns group. Pathological changes of myocardium were identified in all of the LPS groups. The studies suggest that macaques are suitable models for studying endotoxic shock and potential fluid therapies.

[Changes in selectin in early stage of lung injury induced by endotoxic shock in macaque].

OBJECTIVE: To investigate the change in selectin and its effect on lung injury induced by endotoxic [lipopolysaccharide (LPS)] shock in macaque. METHODS: Eleven macaques were randomly divided into two groups: control group (n=5) and LPS group (n=6). The animals of the control group received injection of 1 ml/kg normal saline, and the animals of the LPS group received a dose of 2.8 mg/kg LPS intravenously. The plasma contents of P-selectin and L-selectin were assayed before LPS challenge, 60 and 120 minutes after LPS challenge. Ultrastructure of lung tissue and immunohistochemical assay of P-selectin and L-selectin in the lung were observed. RESULTS: Administration of LPS did not changed P-selectin level in plasma, but decreased the L-selectin level at 120 minutes after LPS challenge in both groups (all P<0.05). By immunohistochemical staining, P-selectin and L-selectin were identified on endothelial cells of alveolar wall of LPS animals, whereas no positive staining of P-selectin and L-selectin was showed in control animals. Damages to alveolar type I and II cells, slight transudation of red blood corpuscles, and damage to the basement membrane were observed with electron microscopy in the endotoxin challenged macaques. No pathological changes were observed in the control group. CONCLUSION: Administration of LPS induces expression of P-selectin and L-selectin in alveolar wall and causes alveolar damages in early-phase of endotoxic shock. In the meantime, the L-selectin and P-selectin in plasma do not change. The selectins play an important role in the pathogenesis of lung injury in the early-phase of endotoxic shock.