Number Of Lipid Inclusions Research Articles

Histological and ultrastructural changes in turkey liver under intensive rear-ing and influence of xenobiotics

Liver problems of various etiologies in turkeys have been reported in many countries for the last 20 years. Poultry dies having no clinical manifestations of the disease, and at pathological autopsy, diffuse haemorrhages and marked dystrophic changes of the organ are noted. To date, there are several factors that can cause such changes, these are unbalanced amino-acid feed, insufficient calcium, biotin, selenium, the very high energy content of feed; zootechnical factors – limited mobility of birds due to cage density violations, high temperature; genetic factors – the influence of estrogens; infectious factors – E. coli, Clostridium, and viruses of Picornaviridae family. The article describes the histopathological and ultrastructural changes in the turkey liver under the influence of various factors. The material for the research was obtained from a farm where turkeys of the “Hybrid Converter” cross are grown, same age, fed with a standard diet that changed according to the technological map of cultivation. On the 50th day of life, a pathological autopsy of the dead poultry was performed, pieces of liver were selected for histological and ultrastructural examination. The visual assessment revealed significantly enlarged liver, the colour from dark red to light brown, flabby consistency. In some cases, diffuse fatty infiltrations of hepatocytes were histologically revealed, in other cases, focal necrosis with the growth of the connective tissue and the formation of massive perivascular couplings were registered. Large vacuolar fatty degeneration of hepatocytes with subsequent development of fibrosis indicates chronic intoxication, probably caused by slow breakdown of fatty acids in cells due to insufficient oxidative phosphorylation, as well as reduced levels of lipotropic factors: choline, methionine and the vitamins. At the ultrastructural level, a large number of lipid inclusions of various sizes, dystrophic changes in mitochondria were observed, which indicates a decrease in the synthetic activity of cells.

СОДЕРЖАНИЕ РЕТИНОЛА И α-ТОКОФЕРОЛА ПРИ ЭКСПЕРИМЕНТАЛЬНОМ ФИБРОЗЕ ПЕЧЕНИ У КРЫС

Background. The content of retinol and α-tocopherol in the human body affects the development and progression of chronic liver diseases and is associated with the functioning of perisinusoidal lipocytes (HSC) and the state of biological membranes. Objective – to evaluate the content of retinol and α-tocopherol in blood plasma and liver tissue in the dynamics of experimental liver fbrosis in rats. Material and methods. Modeling of liver fbrosis / cirrhosis was carried out on sexually mature male rats by intraperitoneal administration of thioacetamide (TAA) solution at a dose of 200 mg / kg every other day for 4 and 12 weeks. The control group of animals received an equal volume of saline. The concentration of α-tocopherol and retinol was determined by S.L. Taylor’s method. Results. In rat liver preparations, 4 weeks after administration of TAA solution to animals, signs of FII-III stage of fbrosis were observed. According to electron microscopy, HSCs were in a transitional state and acquired a more elongated shape; the number of lipid inclusions in their cytoplasm decreased. The administration of TAA for 12 weeks led to the formation of liver cirrhosis in rats, with characteristic macro- and microscopic changes. On light microscopy, the number of HSCs decreased in rat liver preparations 3 months after administration of TAA; activated HSCs were encountered, which acquired an elongated shape and lost lipid inclusions. The content of retinol in the 2nd group of animals (with liver fbrosis stage II-III) was 2.2 times higher than in the control group, and 1.8 times higher than in the 3rd group with liver cirrhosis (p < 0.05). The content of retinol in the liver tissue after 4 weeks of TAA administration decreased by 11.7%, after 12 weeks - by 1.5 times. The level of α-tocopherol in the liver at the stage of fbrosis FII-III decreased by 21% compared with the control group, at the stage of cirrhosis - by 2 times. Conclusion. The use of thioacetamide in rats for 1 and 3 months leads to the development of liver fbrosis and cirrhosis. A decrease in the content of retinol and α-tocopherol in the liver occurs with the progression of liver fbrosis /cirrhosis. The high content of retinol and α-tocopherol in plasma at the stage of liver fbrosis FII-III is due to degranulation (activation) of HSC.

HIV aspartyl peptidase inhibitors interfere with cellular proliferation, ultrastructure and macrophage infection of Leishmania amazonensis.

Background Leishmania is the etiologic agent of leishmanisais, a protozoan disease whose pathogenic events are not well understood. Current therapy is suboptimal due to toxicity of the available therapeutic agents and the emergence of drug resistance. Compounding these problems is the increase in the number of cases of Leishmania-HIV coinfection, due to the overlap between the AIDS epidemic and leishmaniasis.Methodology/Principal FindingsIn the present report, we have investigated the effect of HIV aspartyl peptidase inhibitors (PIs) on the Leishmania amazonensis proliferation, ultrastructure, interaction with macrophage cells and expression of classical peptidases which are directly involved in the Leishmania pathogenesis. All the HIV PIs impaired parasite growth in a dose-dependent fashion, especially nelfinavir and lopinavir. HIV PIs treatment caused profound changes in the leishmania ultrastructure as shown by transmission electron microscopy, including cytoplasm shrinking, increase in the number of lipid inclusions and some cells presenting the nucleus closely wrapped by endoplasmic reticulum resembling an autophagic process, as well as chromatin condensation which is suggestive of apoptotic death. The hydrolysis of HIV peptidase substrate by L. amazonensis extract was inhibited by pepstatin and HIV PIs, suggesting that an aspartyl peptidase may be the intracellular target of the inhibitors. The treatment with HIV PIs of either the promastigote forms preceding the interaction with macrophage cells or the amastigote forms inside macrophages drastically reduced the association indexes. Despite all these beneficial effects, the HIV PIs induced an increase in the expression of cysteine peptidase b (cpb) and the metallopeptidase gp63, two well-known virulence factors expressed by Leishmania spp.Conclusions/SignificanceIn the face of leishmaniasis/HIV overlap, it is critical to further comprehend the sophisticated interplays among Leishmania, HIV and macrophages. In addition, there are many unresolved questions related to the management of Leishmania-HIV-coinfected patients. For instance, the efficacy of therapy aimed at controlling each pathogen in coinfected individuals remains largely undefined. The results presented herein add new in vitro insight into the wide spectrum efficacy of HIV PIs and suggest that additional studies about the synergistic effects of classical antileishmanial compounds and HIV PIs in macrophages coinfected with Leishmania and HIV-1 should be performed.

Ultrastructural Changes in Small Intestinal Lipofibroblasts of Suckling Rabbits with Experimental Cholera

Ultrastructural analysis of the jejunum in suckling rabbits showed that lipofibroblasts localized in the submucosa and adjacent to crypts contain lipid inclusions (granules) with typical "melting" surface. Lipofibroblasts contained moderately widened cisternae of the granular endoplasmic reticulum and few mitochondria with dense matrix and poorly developed cristae. Experimental cholera was usually accompanied by a decrease in the number of lipid inclusions, and only in some cases by accumulation of lipid material. Our results suggest that the material accumulated in granules plays a role in the pathogenesis of cholera.

Magnocellular neuropeptidergic terminals in neurohypophysis: Rapid glial release of enclosed axons during parturition

The ultrastructure of pituicytes as well as their relationship with neurosecretory axons were measured from the following groups of adult rats: virgin females; immediately pre-partum; post-partum; and following 14 days of lactation. Both parturition and lactation brought about a significant decrease in the number of pituicytes with neurosecretory axons completely surrounded by their cytoplasm. Since these two physiological states are each characterized by increased neurohypophysial hormone release, the data suggest that pituicyte enclosure of neurosecretory axons occurs mainly during conditions of low hormone release. Examination of pituicyte size and number of lipid inclusions, and the number of synaptoid contacts from neurosecretory axons onto pituicytes showed no differences among groups.

Electron microscopic studies of Wallerian degeneration in rat optic nerves. I. The multipotential glia.

AbstractThe development of phagocytes has been studied with the electron and light microscopes in rat optic nerves undergoing Wallerian degeneration. The postoperative survival times ranged from five hours to 250 days. This paper focuses on cells that have been designated either as multipotential glia or as a third neuroglial cell type. Such cells increase markedly in number during the first several weeks of nerve fiber degeneration while the populations of astrocytes and oligodendrocytes remain relatively stable. During this early stage of degeneration, multipotential glial cells develop very irregular shapes and have many processes and complex folds that intermingle with the degenerating nerve fibers. These cells engulf myelin fragments and nerve fibers which become enclosed within vacuoles that show acid phosphatase reaction product in specimens prepared for cytochemistry. The debris containing vacuoles can therefore be considered as phagolysosomes. In addition, the multipotential glial cells show an increase in the number of lipid inclusions over that of cells in normal material. Eventually some multipotential glial cells accumulate large quantities of lipid inclusion and come to resemble the “Gitter” cells described in classical neuropathological studies.The numerical and cytological changes occurring within the multipotential glial population indicate that these cells are an important source of phagocytes in the type of lesion which we have studied. The breakdown of degenerating myelin by multipotential glial cells, the origin of these cells and their relationship to the microglial cells stained in light microscopic preparations are discussed in detail.