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ABSTRACT: To explore arsenic-induced oxidative stress and the protective efficacy of α-lipoic acid and vitamin c.
50 male SD rats were randomly divided into 5 groups. Ten rats (the control group) were exposed to deionized water for 6 weeks, and the others were alone exposed to sodium arsenite (50 mg/L water) for 6 weeks, at the same time, three group rats were administered intragastrically (i.g.) with α-lipoic acid 10 mg×kg(-1)×d(-1) and vitamin C 25 mg×kg(-1)×d(-1) either alone or in combination. At the end of experiment, blood was drawn from abdominal aorta, and then the blood, brain and liver of rats were used for biochemical assays, including blood glutathione (GSH), δ-aminolevulinic acid dehydratase (δ-ALAD ), reactive oxygen species (ROS) and oxidized glutathione (GSSG) level. At the same time, the super oxide dismutase (SOD) activity, glutathione peroxidase (GSH-Px) activity, catalase (CAT) activity, ATPase activity of brain and liver were determined. The caspase activity of brain were also determined.
There were a significant increase in ROS level (P < 0.05), but a significant decrease in δ-ALAD activity (P < 0.01) in the chronic arsenic toxicity model group compared with the control group. These alterations were marginally restored by co-administration of vitamin C and α-lipoic acid individually, while significant recovery was observed in the animals supplemented with both the antioxidants together with arsenite in rat (P < 0.05). At the same time, there was a significant increase in the ROS and TBARS level of the brain and liver (P < 0.05), and caspase activity of the brain (P < 0.05), while there was a significant decrease in antioxidant enzymes and ATPase activity on arsenite exposure in rats (P < 0.05). These alterations were also marginally restored by co-administration of vitamin C and α-lipoic acid individually, while significant recovery was observed in the animals supplemented with both the antioxidants together with arsenite in rat (P < 0.05).
Arsenite-induced oxidative stress can be significantly protected by co-administration of α-lipoic acid and vitamin C individually, but the best effects could be observed with combined administration of two antioxidants during arsenite exposure in animals. The dietary intervention of or supplementation with natural dietary nutrients is possible to prevent the effects of arsenic in populations of risk.
Zhonghua lao dong wei sheng zhi ye bing za zhi = Zhonghua laodong weisheng zhiyebing zazhi = Chinese journal of industrial hygiene and occupational diseases 12/2010; 28(12):891-4.
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ABSTRACT: To investigate the change in selectin and its effect on lung injury induced by endotoxic [lipopolysaccharide (LPS)] shock in macaque.
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.
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.
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.
Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 12/2005; 17(12):752-5.
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ABSTRACT: To study changes of inflammation-associated cytokine expressions during early phase of endotoxic shock in macaque.
Experiments were performed in Macaque mulatta treated with LPS 2.8 mg/kg in shock model group or with normal saline in control group. Blood samples were collected before, or 60 min, or 120 min after LPS injection, respectively. Liver and spleen tissues were obtained at 120 min after LPS injection. The plasma levels of TNF-alpha, IL-1beta, IL-10 and IL-12P40 were determined by double-antibody sandwich ELISA with antibodies against human cytokines. The mRNA levels of TNF-alpha, IL-1beta, and IL-18 in peripheral blood mononuclear cells (PBMCs), liver and spleen were examined by real-time fluorescence semi-quantitative RT-PCR with the primers based on human genes.
Mean systemic arterial pressure (MAP), systemic vascular resistance index (SVRI) and left ventricular work index (LVWI) of macaques were significant declined in shock model group on average 60 min after LPS injection. The plasma levels of TNF-alpha and IL-10 were significantly increased 60 min after LPS injection and then decreased. The plasma levels of IL-1beta and IL-12P40 were significantly increased at 120 min after LPS injection. The mRNA levels of TNF-alpha and IL-1beta were significantly increased 60 min after LPS stimulation in PBMCs and 120 min after LPS stimulation in livers. The mRNA level of IL-18 was significantly increased 120 min after LPS stimulation in PBMCs and livers. But in spleen, only TNF-alpha mRNA level in LPS group was significantly higher 120 min after LPS stimulation, compared with that in control group.
An endotoxic shock model of Macaque mulatta was successfully established. Both antibodies for ELISA and PCR primers based on human cytokine assays were successfully applied to detect macaque cytokines. In the model, inflammatory cytokines, such as TNF-alpha, IL-1beta, IL-12 and IL-18 as well as anti-inflammation cytokine IL-10, were released at very early phase of endotoxic shock within 120 min after LPS injection. PBMCs and liver cells might be the important sources of these cytokines.
World Journal of Gastroenterology 11/2004; 10(20):3026-33. · 2.47 Impact Factor
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ABSTRACT: To explore the mechanism of the changes of blood-cerebrospinal fluid barrier in rabbits with diabetic ketoacidosis (DKA).
The New Zealand rabbits were injected with 150 mg/kg streptozotion and alloxan monohydrate each (model group, n=6) intravenously, or equal volume of normal saline (control group, n=6). After 72 hours, blood sugar and uric ketone were detected. All of animals were injected with Evans blue (EB). After 6 hours, arterial blood gases were measured and animals were killed. Absorbency of EB of brain tissue was detected. All brains of animals were examined with light and electron microscopy. Marker of blood-cerebrospinal fluid barrier, cytochemical stains of alkaline phosphatase (ALPase) was operated by ultrastructure. The inducible nitric oxide synthase (iNOS) in brain tissue was detected by immunohistochemical method.
The models of DKA were established after 72 hours of injecting streptozotion and alloxan monohydrate. Absorbency of EB of model group rabbits was slightly increased, but had no significant difference compared with controls (P>0.05). The brain edema, damages of vessel endothelium and necrosis of neuron were observed through histological and ultrastructure examination in model group. ALPase activity of model group was evidently decreased in brain blood vessel endothelium in comparison with controls. Compared to controls, the iNOS activity of model group was increased and its positive cells were aggregated on blood vessel of brain membrane.
By streptozotion and alloxan monohydrate inducing DKA models, NO could induce blood-cerebrospinal fluid barrier damages and result in brain edema.
Zhongguo wei zhong bing ji jiu yi xue = Chinese critical care medicine = Zhongguo weizhongbing jijiuyixue 03/2004; 16(3):175-8.
