Suckling piglets and weaned pigs showed anorexia, dehydration, severe abdominal breathing, emaciation and paresis from Oct. 1993. to Nov. 1993. Five 2-week-old piglets were submitted for diagnosis in Kangwon National University. At necropsy, the pin-point well demarcated yellowish white foci were scattered on the surface of the lung, heart, liver, spleen and kidney. Histologically, multifocal areas of necrosis with mononuclear cells infiltration were found in the lung, heart, liver, lymph node, spleen, kidney and small intestine. These lesions tended to be associated with blood vessels. Variable round to ovoid tachyzoites were located at the periphery of the lesions. The organisms were demonstrated as Toxoplasma gondii by immunohistochemical staining method. Ultrastructurally, this parasite was surrounded with parasitophorous vacuole in alveolar macrophage. The parasite was crescent-shaped and $6{\sim}8{\times}1{\sim}2{\mu}m$ in size. It was enclosed by an thick outer membrane and an underlying thin inner membrane. Several club-shaped paired organelles and conoids lay in the cytoplasm at the anterior. Numerous round body and one to several mitochondria were presented in the cytoplasm. Based on the gross findings, histopathology, immunohistochemical and electron microscopic findings, this case was diagnosed as toxoplasmosis in piglets.
Lipin1 was identified as a phosphatidate phosphatase enzyme, and it plays a key role in lipid metabolism. Since free radicals contribute to metabolic diseases in the liver, this study investigated the effects of free radicals on the regulation of Lipin1 expression in Huh7 and AML12 cells. Hydrogen peroxide induced mRNA and protein expression of Lipin1 in Huh7 cells, which was assayed by quantitative RT-PCR and immunoblotting, respectively. Induction of Lipin1 by hydrogen peroxide was confirmed in AML12 cells. Hydrogen peroxide treatment significantly increased expression of sterol regulatory element-binding protein (SREBP)-2, but not SREBP-1. Moreover, nuclear translocation of SREBP-2 was detected after hydrogen peroxide treatment. Hydrogen peroxide-induced Lipin1 or SREBP-2 expression was significantly reduced by N-acetyl-$\small{L}$-cysteine treatment, indicating that reactive oxygen species (ROS) were implicated in Lipin1 expression. Next, we investigated whether the hypoxic environments that cause endogenous ROS production in mitochondria in metabolic diseases affect the expression of Lipin1. Exposure to hypoxia also increased Lipin1 expression. In contrast, pretreatment with antioxidants attenuated hypoxia-induced Lipin1 expression. Collectively, our results show that ROS activate SREBP-2, which induces Lipin1 expression.
Park, Nam-yong;Ri, Chang-yeong;Chung, Chi-young;Kee, Hye-young;Bae, Seong-yeol
Korean Journal of Veterinary Research
/
v.32
no.1
/
pp.99-109
/
1992
Pathological studies by light and electron microscope were carried out on the twenty piglets naturally affected by encephalomyocarditis virus infection. Gross findings included pale or yellow, small necrotic foci on myocardium, together with pulmonary edema and liver congestion in some cases. On light microscopy, nonsuppurative interstitial endocarcitis, epicarditis and myocarditis, myocardial infarction, and dystrophic calcification or fibtosis were observed in heart. Perivascular cuffings, gliosis and nonsuppurative meningitis were appeared in brain. Focal or diffuse necrosis with mononuclear cell infiltration in lacrimal gland and multifocal necrosis in liver were observed in some cases. Congestion and edema of lung, hyperemia, hemorrhage and deletion of lymphocytes of lymph nodes and spleen were recognized. On electron microscopy, severe swelling and vacuolization of mitochondria and sarcoplasmic reticulum, large intracellular vacuolation and edema, separation and fragmentation of myofibrils were observed. Virus particles were seen in the sarcoplasm of degenerated cardiac muscle cell.
Kim, Tae-Hoon;Ahn, Hee-Young;Kim, Young-Wan;Sim, So-Yeon;Seo, Kwon-Il;Cho, Young-Su
Journal of Life Science
/
v.28
no.6
/
pp.697-707
/
2018
The aim of this study was to investigate the potential effects of extracts from silkworm (Bombyx mori L.) that was fermented with Bacillus subtilis KACC 91157 at the levels of 1%(v/w), 2.5%(v/w), and 5%(v/w) in alcohol-fed rats. Sprague-Dawley rats were divided into seven groups: normal group (N), alcohol treated group (C), silymarin treated group (PC, positive control), 5% silkworm powder treated group (SP5), 1% Bacillus subtilis-fermented silkworm powder treated group (BSP1), 2.5% BSP treated group (BSP2.5), and 5% BSP treated group (BSP5). The activities of AST, ALT, ALP, and LDH in the serum and the triglyceride concentrations in the liver and serum were increased by alcohol feeding but were reduced in the BSP5 group. In addition, the contents of total lipids, free fatty acids, and total cholesterol were increased in the alcohol-fed group but were reduced in the BSP5 group. The activities of ADH, ALDH and ADH, ALDH protein levels in the liver were increased in the BSP5 group. The TBARS contents in the liver, serum, liver mitochondria, and liver microsomes were slightly decreased in the BSP5 group compared to the C group. The hepatocytes in alcohol-fed rats contained numerous large droplets; however, BSP5 treatment prevented alcohol-induced lipid droplet accumulation in the hepatocytes. Based on these results, extracts from Bacillus subtilis-fermented silkworm (Bombyx mori L.) have significant potential for development into a functional health food that can improve alcoholic fatty liver conditions.
An, Mi-Jung;Suh, Jung-Soon;Lee, In-Ja;Cho, Sung-Hee
Journal of the Korean Society of Food Science and Nutrition
/
v.14
no.2
/
pp.145-150
/
1985
This study was conducted to examine the pharmacological effect of water soluble extract of Lichens (Parmelia, Physcia and Cladonia species) on liver-damaged rat by $CCl_4$ injection. Rat livers were damaged acutely and chronically by one-time injection of $CCl_4$ just prior to five days of experimental period and continuous injections in every three days for eight weeks of experimental period, respectively. During each period the experimental group was fed Lichens extract(5.5 mg of dry wt/ml) instead of water given to the control group. For both acute and chronic liver damage, the experimental group showed higher oxidative activity of hepatic mitochondria measured by state 3 respiration, P/O ratio, respiratory control and ATP synthesized, compard to the control group. Serum glucose was slightly higher in the experimental group but liver glycogen showed no significant difference between experimental and control groups. In experimental group, liver glucose-6-phosphatase activity was increased during first two days after acute liver damage, but not significantly different from control group during chronic damage. Liver lactate, malate plus fumarte and glutamate tended to be higher in the experimental group, especially for chronic liver damaged rat. It is concluded that Lichens extract stimulate cytoplasmic and mitochondrial oxidative activities and the possible mechanism of the latter is supposed to involve the preservation of membrane integrity by certain component(s) of water-soluble Lichens extract.
This study aims to demonstrate the effect of chitosan oligosaccharide on the ultrastructural changes in the mouse liver toxicated by carbon tetrachloride $(CCl_4)$. A healthy male ICR mouse that weighted $27{\pm}2gm$ was used for experiment. The experimental group was divided into three groups; the group A; the pretreated group with chitosan oligosaccharide, the group B; the simultaneous group, the group C; treated only the $CCl_4$. The group A was simultaneously treated with chitosan oligosaccharide and $CCl_4$ after pretreated with chitosan oligosaccharide for 7 days. The group B injected $CCl_4$ and chitosan oligosaccharide to the intraperitoneal. The group C injected with only $CCl_4$ to the intraperitoneal. The results were as follow: In the group A, the nuclear membrane and the mitochondria were observed almost normal in shapes at overall the time. Some lamellae of the RER (rough endoplasmic reticulum) destructed until 48 hours but ribosome attached. The destructed lamellae reformed at 72 hours but the smooth membrane vesicles not observed. The lysosomes observed at 72 hours. At 96 hours, all organelles showed in normal shapes. In the group B, changes of nuclear membranes were relatively lighter than group C. Mitochondria observed normal shape through the time. Parts of RER reformed the lamellae, other parts dilated inner cavity. And lipid droplet observed around the 24 hours. Glycogen and lysosome observed 48 hours and 72 hours, respectively. In the group C, nuclear membrane was irregular and nuclear cytoplasm condensed through the time. The lamellae of RER destructed from 24 to 96 hours. Smooth membrane vesicles observed in the cytoplasm at 48 ours. Mitochondria was less effected by toxic. And from the 24 hours, the variable sizes of lipid droplets observed in tile cytoplasm. These results suggest that chitosan oligosaccharide attenuates the toxic effect of the carbon tetrachloride in the mouse liver.
This study was to investigate the effect of selenium on hepatic antioxidative defense system and oxidative damage in lead-administered rats. Male Sprague-Dawley rats weighing 140$\pm$5g were divided into one normal group(Se, 0 ppm) and three lead groups according to dietary levels of selenium supplementation: Pb0(Se, 0 ppm), PbS(Se, 0.5 ppm), and PbSS(Se, 1.0 ppm). All experimental groups were fed the experimental diet ad libitum for 4 weeks, and lead groups fed one containing 2,000 ppm lead acetate. Liver superoxide dismutase(SOD) activities in Pb0 group increased compared with other experimental groups. Liver gluthathione peroxidase(GSH-px) activities in Pb0 group decreased compared with normal group, but those of PbS and PbSS groups significantly increased compared with Pb0 group. Glutathione S-transferase(GST) activities decreased in Pb0 group and not significantly different from PbS and PbSS groups compared with normal group. Reduced glutathione(GSH) contents and GSH/GSSG of liver in Pb0 group were lower than those of other groups. Liver vitamin E contents in Pb0 group were about 50% of the normal group, but those of PbSS and PbS increased more than Pb0 group. Liver damage in electron microphotography process decreased in RER, showed an increase in Iysosome and also an increase in swelling of mitochondria. and ordered as follows : PbSS. PbS. and Pb0. It was concluded that high levels of dietary selenium had protective effects on peroxidative damage of hepatic cell accompanied with increased antioxidative defense system in lead-administered rats.
It has been well documented that animals exposed to cold show increased activity of thyroid gland. The calorigenic action of thyroid hormone has been demonstrated by a variety of in vivo and in vitro studies. According to Edelman et al., the thyroid thermogenesis is due to activation of energy consuming processes, especially the active sodium transport by the hormone in target tissues. If so, the increase in thyroid activity during cold exposure should induce increased capacity of sodium transport in target tissue and the change in tissue metabolism should be precisely correlated with the change in Na+_K+_ATPase activity of the tissue. This possibility was tested in the present study: in one series, changes in oxygen consumption and Na+_K+_-ATPase activity of liver preparations were measured in rats as a function of thyroid status, in order to establish the effect of thyroid hormone on the tissue respiration and enzyme system in another series, the effect of cold stimulus on the serum thyroid hormone level, hepatic tissue oxygen consumption and Na+_K+_ATPase activity in rats. The results obtained are as follows: 1. The Na+_dependent oxygen consumption of liver slices, the oxygen consumption of liver mitochondria and the Na+_K+_ATPase activity of liver preparations were significantly inhibited in hypothyroidism and activated in hyperthyroidism. Kinetic analysis indicated that the Vmax. of Na+_K+_ATPase was decreased in hypothyroidism and increased in hyperth)'roidism. 2. In cold exposed rats, the serum triiodothyronine (T₃) level increased rapidly during the initial one day of cold exposure, then declined slowly to the control level after two weeks. The serum thyroxine (T₄) level decreased gradually throughout the cold exposure. Accordingly the T₃/T₄ratio increased. The mitochondrial oxygen consumption and the Na+_dependent oxygen consumption of liver slices increased during the first two days and then remained unchanged thereafter The activity of the Na+_K+_ATPase in liver preparations increased during cold exposure with a time course similar to that of oxygen consumption. Kinetic analysis indicated that the Vmax. of Na+_K+_ATPase increased. 3. Once the animal was adapted to cold, induction of hypothyroidism did not significantly alter the hepatic oxygen consumption and Na+_K+_ATPase activity. These results indicate that: 1) thyroid hormone increases capacities of mitochondrial respiration and active sodium transport in target tissues such as liver; 2) the increased T₃level during the initial period of cold exposure facilitates biosynthesis of Na+_K+_ATPase and mitochondrial enzymes for oxidative phosphorylation, leading to enhanced production and utilization of ATP, hence heat production.
An enzyme that hydrolyzes flavin-adenine dinucleotide (FAD) was found to be present in rat liver lysosomal membrane prepared from Triton WR-1339 filled lysosomes (tritosomes) purified by flotation on sucrose. This FAD phosphohydrolase (FADase) exhibited optimal activity at pH 8.5 and had an apparent Km of approximately 3.3 mM. The activity was decreased 50~70% by dialysis against EDTA and this was restored by $Zn^{2+}$, $Mg^{+2}$, $Hg^{+2}$, and $Ca^{+2}$ ions inhibited the enzyme, but $F^-$ and molybdate had no effect. The enzyme was also inhibited by p-chloromercuribenzoate (pCMB), reduced glutathione and other thiols, cyanide, and ascorbate. The presence of ATP, ADP, AMP. ${\alpha}-{\beta}-methylene$ ATP, AMP-p-nitrophenyl phosphate (PNP), GMP, and coenzyme A (CoA) decreased the activity on FAD, but pyrimidine nucleotides, adenosine, adenine, or $NAD^+$ were without effect. Phosphate stimulated the activity slightly. FAD phosphohydrolase activity was separated from ATPase and inorganic pyrophosphatase activities by solubilization with detergents and polyacrylamide gel electrophoresis and by linear sucrose density gradient centrifugation suggesting that the enzyme is different from ATPase, inorganic pyrophosphatase, and soluble lysosomal FAD pyrophosphatase. Paper chromatography showed that FAD was hydrolyzed to flavin mononucleotide (FMN) and AMP which were further hydrolyzed to riboflavin and AMP by phosphatases known to be present in lysosomal membranes. Incubation of the intact Iysosomes with pronase showed that the active site of FAD phosphohydrolase must be oriented to the cytosol. The FAD hydrolyzing activity was detected in Golgi, microsome, and plasma membrane, but not in mitochondria or soluble lysosomal preparations.
To investigate the effect of the squalene against the lead toxicity. A healthy male of ICR mice were used for experiment. The SOD was observed after the intraperitoneal injection in mice. The ultrastructural changes of the liver were observed after the intraperitoneal injection in mice. The experimental groups were divided into two groups. Group A was control group that squalene was not treated after intraperitoneal injection of lead acetate. Group B was squalene treatment group that squalene solution was injected after intraperitoneal injection of lead acetate. All groups were used to 10 mice. The results were as follow: SOD activity in the liver, Group A was lower than in normal. But, Group B was higher than in Group A (P<0.05). In the histological observation, Group A were showed that the inner cavity of mitochondria swellen and development of cristae weakened. Swelling of lamellae of rough endoplasmic reticulum (rER) was showed. It was concluded that the SQ will be effective for the recovery of hepatic cell at lead intoxication.
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