Single Exposure Of Rats Research Articles

Изучение последствий острых поражений веществами пульмонотоксического действия

Цель исследования - изучение особенностей развития последствий острого поражения веществами пульмонотоксического действия. Методика. Исследование выполнено на 160 белых нелинейных крысах-самцах массой 180-220 г. Для оценки развития последствий острого поражения пульмонотоксикантами использовали модели отравления фосгеном, диоксидом азота и паракватом. Проводили оценку гравиметрических показателей легочной ткани и изменений толерантности к физической нагрузке по показателю продолжительности плавания «до отказа» с грузом 7% от массы тела животного. Также проводилась морфологическая оценка тяжести поражения ткани легких. Результаты. Установлено, что однократное поражение крыс пульмонотоксикантами в дозе 1LCt в остром периоде сопровождается развитием комплекса морфологических и функциональных изменений, характерных для токсического отека лёгких. У части животных наблюдалось выраженное снижение функциональных возможностей, патологоанатомическим субстратом которых являлось нарушение структуры легочной паренхимы с деструкцией и фиброзированием бронхов и сосудов, развитием выраженной панацинарной эмфиземы, которая в 35% случаев сочетается с хроническими гнойно-деструктивными изменениями в легочной ткани. Заключение. Частота развития необратимых последствий поражений веществами пульмонотоксического действия составила: 60% случаев при отравлении паракватом, 40 и 20% при поражении фосгеном и диоксидом азота соответственно. The purpose is to study features of an acute injury progression in case of poisoning by agents of pulmonotoxic action. Experimental work was done in a model of 160 white non-linear male rats weighing 180-220 g. For the assessment of an acute injury development after poisoning by agents of pulmonotoxic action the models of phosgene, nitrogen dioxide and paraquat poisoning were used. The assessment of gravimetric characteristics of lung tissue and changes of physical activity tolerance according to the rate of swimming duration to the full with 7%-load of body mass was carried out. The morphological assessment of severity of lung tissue injury was carried out as well. Results. It was found out that a single exposure of rats with pulmonotoxicants in 1LCt during its acute period was accompanied by the development of a range of morphological and functional changes which were typical for the course of toxic pulmonary edema. As a consequence of poisoning in a half of animals an evident decrease of functional abilities was observed. Pathologicoanatomic substrate of these abilities was the abnormality of lung parenchyma with destruction and bronchial tube and vessel fibrosis, that in 35% of cases matched with chronical purulent-destructive changes in lung tissue. Conclusion. The rate of consequences development after pulmonotoxic agents exposure was the following: 60% cases after paraquate exposure, 40% and 20% after phosgene and nitrogen dioxide respectively.

랫드를 이용한 Burkholderia pyrrocinia CAB08106-4의 급성경구, 호흡기, 정맥독성/병원성시험

Abstract Burkholderia pyrrocinia CAB08106-4 has an anti-bacterial effect on Garlic White Rot caused bySclereotium cepivorum and Sclereotium sp.. It is an environmentally friendly microbial product that preventsand controls a variety of phytopathogens involving Garlic White Rot caused by Sclereotium cepivorum andSclereotium sp.. The aim of this study was to assess and to compare the pathogenicity of Burkholderiapyrrocinia CAB08106-4 by single exposure of rats through several routes such as oral, intranasal andintravenous. For the acute toxicity / pathogenicity study, the animals were sacrificed on days 3, 7, 14 and 21,and macroscopically observed their organs to examine the numbers of internally-retained pesticidal microbes.Clinical examinations were performed daily during administration period, and body weight gain wasevaluated. In the study, no clinical sign, weight gain and mortality were observed in relation to theadministration of test article. The significant changes of internal/external microbes by test article were notdetected. The pathological findings in relation to the administration of the test article in the necropsy werenot observed. It could be concluded that the microorganism was not toxic or pathogenic in rats via oral,intranasal and intravenous route. Keywords Burkholderia pyrrocinia CAB08106-4, Garlic disease, Intranasal, Intravenous, Oral, Pathogenicity

Влияние ионизирующей радиации на ферментные активности и состояние ядерно-ядрышкового аппарата гепатоцитов крыс

The effects of a single exposure of rats to the whole-body roentgen irradiation at the doses of 3.5 Gy and 4.5 Gy on the activity of creatine kinase, purine nucleoside phosphorylase, alanine aminotransferase, aspartate aminotransferase, as well as on the state of the nuclear-nucleolar apparatus in rat hepatocytes on the 6th and 13th days after radiation exposure have been studied. Irradiation at the above doses induced changes in the levels of enzymatic activity of different values and different directions within the same time periods, as well as oscillating changes in this type of enzymatic activity over time. This demonstrates various radiosensitivity and adaptation abilities of these enzymatic activities. The changes in the enzymatic activity significantly correspond to the changes in the morphometric indices of nuclear-nucleolar apparatus of hepatocytes, as well as the distribution of hepatocytes within the ploidy classes: in particular, stabilization of the enzymatic activity on the 13th day after irradiation correlates with the increased transcriptional activity, which is detectable through the increased number of nucleoli per nucleus and the expanded space of a hepatocyte nucleus. The compensation mechanisms are likely to be targeted at the changes in the functional activity of surviving hepatocytes, rather than at the replacement of the damaged cells by the new ones.

Mechanisms underlying the long-term behavioral effects of traumatic experience in rats: The role of serotonin/noradrenaline balance and NMDA receptors

Traumatic stressors induce long-lasting changes in behavior. It is believed that all three glutamatergic, serotonergic and noradrenergic neurotransmission play a role in the development of such behavioral changes, but their relative importance and relationship is poorly understood. We have shown previously that a single exposure of rats to electric shocks induces social avoidance for about 10 days. Here we assessed social avoidance 24 h after shock exposure in rats with chemically lesioned serotonergic and noradrenergic neurons. The effects of the NMDA receptor blocker MK-801 were also studied. When the serotonin/noradrenaline balance was shifted towards serotonergic dominance via chemical lesions, the behavioral dysfunction was markedly attenuated. The disruption of serotonergic neurotransmission (that lead to noradrenergic dominance) significantly increased the behavioral deficit. Shock responding was not secondary to lesion-induced differences in social behavior. Noteworthy, the brain noradrenaline/serotonin ratio correlated negatively with shock-induced social avoidance, suggesting that the ratio rather than absolute levels are important in this respect. In line with this assumption, double lesions had minor effects on social avoidance, suggesting that these monoaminergic systems modulate, but do not mediate the behavioral deficit. The blockade of NMDA receptors abolished the development of stress-induced social avoidance both when applied before shocks and when applied before behavioral testing. We confirmed that the long-term behavioral effects of traumatic experience result from glutamatergic activation, the effects of which are mediated by NMDA receptors. The development of the behavioral deficit is modulated by the balance between serotonergic and noradrenergic neurotransmission, possibly via effects on shock-induced glutamatergic activation.

Effects of nitrogen dioxide on lactic dehydrogenase isozymes.

STUDIES of alterations in enzyme activity levels in lung tissues resulting from inhalation of noxious agents have revealed that these changes tend to occur early and may precede clinical signs of tissue damage. Kilroe-Smith and Breyer1 found that succinodehydrogenase and succinoxidase activity levels were increased and cytochrome c oxidase levels decreased in guinea pig lung exposed to silica dust before the usual increase in collagen formation occurred. A single exposure of rats and mice to ozone resulted in lower alkaline phosphatase and succinic dehYdrogenase activity in the lung and elevated levels in serum.2 However, intermittent exposures (one to three times weekly) induced elevated lung and serum alkaline phosphatase. The conditions of exposure as well as the type of irritant apparently plays a part in the enzyme response. The work of Scheel et alB indicates that alkaline phosphatase and 5'-nucleotidase activity levels were depressed following in vivo ozone exposure. Oxygen consumption of the whole animal was depressed by the ozone exposure. Oxygen consumption, lactic dehydrogenase (LDH) and aldolase enzyme levels were determined in this laboratory in lung, liver, kidney and spleen tissue homogenate following acute and chronic exposure of guinea pigs to nitrogen dioxide and were found to be elevated in all tissues.4 The existence of characteristic tissue patterns is well