Effect of benz(a)pyrene and constant light exposure on rat liver lysosomes and biliary excretion of lysosomal enzymes

Пупышев, А. Б.; Gutina, E. M.; Fedina, R. G.; Мичурина, С. В.; Shurlygina, A. V.; Verbitskaya, L. V.

doi:10.1007/s10517-005-0205-6

Cited by 5 publications

(2 citation statements)

References 11 publications

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“…Нами отмечено, что при воздействиях БаП желчные капилляры расширяются, их микроворсинки неравномерно утолщаются. Имеются данные о повышении активности фермента N-ацетил-b, D-глюкозаминидазы в желчи крыс после введения БаП, индуцирующего выброс ферментов лизосом в желчь [9]. По-видимому, при воздействии БаП происходит перестройка путей везикулярного транспорта в гепатоцитах, способствующая ускорению выведения органических анионов из клеток печени в желчь, вероятно, направленная на активное удаление БаП и его метаболитов из гепатоцитов.…”

Section: рис 3 ультраструктурные изменения в гепатоцитах крыс послеunclassified

Liver and Its Lymph Region at Benzo[a]pyrene Effects in an Experiment

Мичурина

Бородин²,

Kolesnikov

et al. 2015

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Liver and Its Lymph Region at Benzo[a]pyrene Effects in an Experiment Background: Benzo[a]pyrene (BaP) is the widespread environmental toxicant with carcinogenic activity. BaP undergoes metabolic activation in the liver microsomal monooxygenase system, and its regional lymph nodes act as peripheral filters, purifying lymph formed in the liver. It remains an open question about the significance of the integral liver and lymphatic system work in supporting processes of adaptation and resistance to the BaP effects. Objective: The purpose of our investigation was to study structural and metabolic changes in the liver and its lymph region in males Wistar rats weighing 180-220 g. Methods: Animals of the experimental group (n =20) daily for 3 days was performed BaP injections: intraperitoneal with 2 mg per 100 g of body weight in 0.2-0.3 ml of olive oil. Rats in the control group (n =20) received in the same mode of injection of olive oil. The light and electron microscopy morphometric study of the liver and its regional lymph nodes morphometric analysis were performed. The intensity of lipid peroxidation in the liver was measured by the number of diene conjugates (DC), ketotriene conjugates (KC) and malondialdehyde (MDA). Results: Simultaneous increase of the hepatic sinusoids relative area and the specific area of the regional lymph nodes sinus system under the BaP effect was found. At ultrastructural level dilatation of the Disse spaces, filling of cell detritus and collagen fibers bundles of these spaces were noted. Damage of nuclear apparatus, balloon transformation of granular endoplasmic reticulum profiles were found in hepatocytes, condensation of the mitochondrial matrix was observed. The relative squares of B-dependent zones increased and T-dependent paracortical zone reduced in the regional lymph nodes. The increase in the content of KC and MDA in liver was identified. Conclusion: benzo[a]pyrene causes interrelated cascade of reactions in the liver and in its lymphatic region: a disturbance of the blood-lymph barrier morphological organization, and so obstruction of the lymphatic drainage from the organ. These promotes development of tissue hypoxia and apoptosis, protein synthesizing and energy cell apparatus disruptions, formation of lymphoid tissue temporary infiltrates in the liver.

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Section: рис 3 ультраструктурные изменения в гепатоцитах крыс послеunclassified

Liver and Its Lymph Region at Benzo[a]pyrene Effects in an Experiment

Мичурина

Бородин²,

Kolesnikov

et al. 2015

ARAMS

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“…Data are presented as M ± m, n = 5-6 per group. Autophagy activation was measured by permeabilization of lysosomal membranes as an increment of free activity of β-galactosidase (in percentage of the total activity of the enzyme) after treatment of brain homogenate in hypotonic media as described in (Pupyshev et al, 2005). Ceftriaxone (100 mg/kg/day for 5 weeks, intraperitoneally) was applied as a neuroprotective treatment since it demonstrated a marked neuroprotective potential at experimental neurodegeneration in the models of Parkinson's and Alzheimer's disease (Weng et al, 2016;Tikhonova et al, 2017).…”

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confidence: 99%

The regulatory role of cystatin C in autophagy and neurodegeneration

et al. 2019

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Autophagy is a dynamic cellular process involved in the turnover of proteins, protein complexes, and organelles through lysosomal degradation. It is particularly important in neurons, which do not have a proliferative option for cellular repair. Autophagy has been shown to be suppressed in the striatum of a transgenic mouse model of Parkinson’s disease. Cystatin C is one of the potent regulators of autophagy. Changes in the expression and secretion of cystatin C in the brain have been shown in amyotrophic lateral sclerosis, Alzheimer’s and Parkinson’s diseases, and in some animal models of neurodegeneration, thus proving a protective function of cystatin C. It has been suggested that cystatin C plays the primary role in amyloidogenesis and shows promise as a therapeutic agent for neurodegenerative diseases (Alzheimer’s and Parkinson’s diseases). Cystatin C colocalizes with the amyloid β-protein in the brain during Alzheimer’s disease. Controlled expression of a cystatin C peptide has been proposed as a new approach to therapy for Alzheimer’s disease. In Parkinson’s disease, serum cystatin C levels can predict disease severity and cognitive dysfunction, although the exact involvement of cystatin C remains unclear. The aim: to study the role of cystatin C in neurodegeneration and evaluate the results in relation to the mechanism of autophagy. In our study on humans, a higher concentration of cystatin C was noted in cerebrospinal fluid than in serum; much lower concentrations were observed in other biological fluids (intraocular fluid, bile, and sweat). In elderly persons (61–80 years old compared to practically healthy people at 40–60 years of age), we revealed increased cystatin C levels both in serum and intraocular fluid. In an experiment on C57Bl/6J mice, cystatin C concentration was significantly higher in brain tissue than in the liver and spleen: an indication of an important function of this cysteine protease inhibitor in the brain. Using a transgenic mouse model of Parkinson’s disease (5 months old), we demonstrated a significant increase in osmotic susceptibility of brain lysosomes, depending on autophagy, while in a murine model of Alzheimer’s disease, this parameter did not differ from that in the appropriate control.

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