Редокс-реакции у Hydrocharis morsus-ranae L. в условиях техногенной нагрузки

Aquatic ecosystems are very sensitive to industrial impacts, and, therefore, it is increasingly important to study the mechanisms underlying the tolerance of aquatic organisms to water pollution. Heavy metals (HMs) are among the most common and toxic pollutants of aquatic ecosystems. They have a particularly strong effect on macrophytes, which are in close contact with the aquatic environment and can accumulate metals in considerable quantities. Hydrocharis morsus-ranae L. is a floating macrophyte (pleistophyte) with a high capacity for accumulation of HMs. The aim of the present study was to assess the effect of industrial pollution on the redox reactions in H. morsus-ranae and to identify the role of low molecular weight antioxidants in adaptation of this macrophyte to unfavorable conditions. A comparative analysis of the physiological and biochemical characteristics of H. morsus-ranae from two (reference and impacted) water bodies was carried out. The study revealed an increased level of lipid peroxidation products in the leaves of H. morsus-ranae under industrial impact, which indicates oxidative stress. Nevertheless, this floating plant demonstrated fairly high resistance to adverse conditions, due to the synthesis of non-enzymatic antioxidants such as proline and soluble protein thiols. Revealing the response of macrophytes to pollution of water bodies will help predict the state of aquatic ecosystems with an increase in anthropogenic pressureВодные экосистемы характеризуются высокой чувствительностью к техногенным нагрузкам, поэтому все более актуальным является изучение механизмов устойчивости гидробионтов к загрязнению водных объектов. Тяжелые металлы (ТМ) относятся к наиболее распространенным и токсичным поллютантам гидроэкосистем. Особенно сильное воздействие они оказывают на макрофиты, которые контактируют с водной средой и могут накапливать металлы в значительных количествах. Hydrocharis morsus-ranae L. относится к плавающим макрофитам (плейстофитам), обладающим высокой аккумулятивной способностью по отношению к ТМ. Цель исследования – оценка влияния техногенного загрязнения на редокс-реакции у H. morsus-ranae, а также выявление роли низкомолекулярных антиоксидантов в его адаптации к неблагоприятным условиям. Проведен сравнительный анализ физиолого-биохимических характеристик H. morsus-ranae из двух водных объектов (фон и импакт). Исследование определило повышенный уровень содержания продуктов перекисного окисления липидов в листьях H. morsus-ranae в условиях техногенного воздействия, что свидетельствует об окислительном стрессе. Тем не менее этот макрофит продемонстрировал достаточно высокую устойчивость к неблагоприятным условиям, что стало возможным благодаря синтезу таких неэнзиматических антиоксидантов, как пролин и растворимые белковые тиолы. Выявление ответных реакций макрофитов на загрязнение водных объектов будет способствовать прогнозированию состояния гидроценозов при усилении антропогенного прессинг

Signaling Pathways Potentially Responsible for Foam Cell Formation: Cholesterol Accumulation or Inflammatory Response—What is First?

Accumulation of lipid-laden (foam) cells in the arterial wall is known to be the earliest step in the pathogenesis of atherosclerosis. There is almost no doubt that atherogenic modified low-density lipoproteins (LDL) are the main sources of accumulating lipids in foam cells. Atherogenic modified LDL are taken up by arterial cells, such as macrophages, pericytes, and smooth muscle cells in an unregulated manner bypassing the LDL receptor. The present study was conducted to reveal possible common mechanisms in the interaction of macrophages with associates of modified LDL and non-lipid latex particles of a similar size. To determine regulatory pathways that are potentially responsible for cholesterol accumulation in human macrophages after the exposure to naturally occurring atherogenic or artificially modified LDL, we used transcriptome analysis. Previous studies of our group demonstrated that any type of LDL modification facilitates the self-association of lipoprotein particles. The size of such self-associates hinders their interaction with a specific LDL receptor. As a result, self-associates are taken up by nonspecific phagocytosis bypassing the LDL receptor. That is why we used latex beads as a stimulator of macrophage phagocytotic activity. We revealed at least 12 signaling pathways that were regulated by the interaction of macrophages with the multiple-modified atherogenic naturally occurring LDL and with latex beads in a similar manner. Therefore, modified LDL was shown to stimulate phagocytosis through the upregulation of certain genes. We have identified at least three genes (F2RL1, EIF2AK3, and IL15) encoding inflammatory molecules and associated with signaling pathways that were upregulated in response to the interaction of modified LDL with macrophages. Knockdown of two of these genes, EIF2AK3 and IL15, completely suppressed cholesterol accumulation in macrophages. Correspondingly, the upregulation of EIF2AK3 and IL15 promoted cholesterol accumulation. These data confirmed our hypothesis of the following chain of events in atherosclerosis: LDL particles undergo atherogenic modification; this is accompanied by the formation of self-associates; large LDL associates stimulate phagocytosis; as a result of phagocytosis stimulation, pro-inflammatory molecules are secreted; these molecules cause or at least contribute to the accumulation of intracellular cholesterol. This chain of events may explain the relationship between cholesterol accumulation and inflammation. The primary sequence of events in this chain is related to inflammatory response rather than cholesterol accumulation