Об определяющей роли биологических факторов в коррозии сплава Д16Т. Обзор
Аннотация
Изучена биокоррозия дюралюминия марки Д16Т и предложен механизм, согласно которому инициаторами начальных коррозионных повреждений являются активные формы кислорода (АФК), продуцируемые микромицетами. Сделано предположение об участии в микологической коррозии сплава Д16Т пероксида водорода, образующегося как в процессе жизнедеятельности микромицетов, так и при активации кислорода нульвалентным алюминием (ZVAl). Предложены механизмы межкристаллитной, питтинговой и язвенной коррозии дюралюминия в условиях воздействия микроскопических грибов. Цель статьи - Определение основного биологического фактора,
инициирующего биокоррозию сплава Д16Т; оценка биологического воздействия ассоциации микроскопических грибов на сплав с целью разработки научно обоснованных и эффективных методов защиты алюминия и его сплавов от биокоррозии микромицетами.
Объектом исследования был выбран сплав алюминия Д16Т в соответствии с ГОСТ 4784-2019 после закалки и естественного старения, широко применяющийся для изготовления силовых элементов конструкций и оборудования топливных систем самолетов, кузовов автомобилей, деталей различных машин и агрегатов, работающих при низких температурах, в пищевой и фармацевтической промышленности. С помощью сканирующего электронного микроскопа изучены стадии инициирования и развития биокоррозии сплава Д16Т в условиях воздействия консорциума плесневых грибов. Изучен фазовый состав продуктов коррозии Д16Т.
В процессе жизнедеятельности микроскопических грибов образуются активные формы кислорода, инициирующие биокоррозию сплава Д16Т. Начальная стадия биокоррозии обусловлена гидролизом защитной пассивной пленки алюминия. На стадии интенсивной биокоррозии образуются кислородсодержащие соединения алюминия в виде водонасыщенного геля. Далее происходит наработка этого продукта коррозии и уменьшение его водопроницаемости. Гель подвергается «старению» и превращается в кристаллические продукты. Конидии и гифы микроскопических
грибов адгезируются, механически закрепляются на поверхности металла и проникают в поверхностные слои и вглубь металла, вызывая его коррозионные разрушения в виде питтингов, язв и каверн. Не исключено, что инициирование биокоррозии металлов является следствием гиперпродукции клетками микромицетов активных форм кислорода в результате окислительного стресса. Это может являться их защитной стратегией, направленной на разрушение ксенобиотического материала.
Развитие межкристаллитной и точечной (питтинговой) коррозии сплава Д16Т под действием микромицетов происходит в местах контакта с экссудатом, который за счет протекания каскада реакций с участием АФК локально обогащается гидроксид-ионами. Зарождение и развитие питтинга на поверхности дюралюминия протекает в дефектах пассивной оксидной пленки вследствие вытеснения кислородсодержащих поверхностных соединений алюминия и их взаимодействия с коррозионно-активными анионами OH– и АФК. Пероксид водорода, как промежуточный продукт метаболизма микромицетов, на поверхности сплава Д16Т может участвовать в фентоновском процессе или гетерогенно разлагаться, также провоцируя развитие биокоррозии алюминия.
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