Экспрессия генов CDKN1A, MDM2 и ATM как биомаркер токсического действия тяжёлых металлов (обзор литературы)

Разработка новых подходов, которые позволят дифференцировать широкий спектр токсических эффектов, поможет значительно улучшить оценку риска. Для понимания механизмов ответа на молекулярном уровне важно изучение экспрессии генов, отвечающих за репарацию ДНК, так как данный процесс является одним из ранних ответов на токсическое действие.

Цель исследования — обобщение имеющихся данных об экспрессии генов репарации (CDKN1A, MDM2 и ATM) в рамках токсического эффекта воздействия тяжёлых металлов.

Проведён систематический поиск для выявления исследований по заданной теме в электронных базах данных PubMed, Web of Science, eLIBRARY и Google Scholar. Для поиска использовались следующие ключевые слова: heavy metals, CDKN1A, MDM2, ATM, toxicity, DNA repair, gene expression. Поиск научных публикаций осуществлялся независимо тремя авторами, все найденные статьи проверялись и сравнивались для отсеивания дублирующихся статей. В данный обзор включено 50 литературных источников.

Анализ токсикогеномных исследований позволил выделить несколько генов для оценки токсичности тяжёлых металлов среди большого количества биомаркеров-кандидатов. Наиболее часто рассматриваемыми генами являются ген p21/CDKN1A, протоонкоген MDM2 и ген ATM.

Ограничения исследования. Ограничением данного обзора является рассмотрение изменения экспрессии лишь небольшого числа генов, отвечающих за репарацию ДНК.

Заключение. Таким образом, экспрессия вышеперечисленных генов биомаркеров даёт детальную картину реакции биологической системы на воздействие вредных факторов и может применяться в рамках оценки токсического действия.

Участие авторов. Все соавторы внесли равнозначный вклад в исследование и подготовку статьи к публикации, прочли и одобрили финальную версию перед публикацией.

Конфликт интересов. Авторы декларируют отсутствие явных и потенциальных конфликтов интересов в связи с публикацией данной статьи.

Финансирование. Исследование не имело спонсорской поддержки.

Поступила: 09.10.2023 / Принята к печати: 15.11.2023 / Опубликована: 08.12.2023

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