Biopolym. Cell. 2017; 33(1):3-23.
http://dx.doi.org/10.7124/bc.000943
Огляди
Аберрантна ДНК глікозілазная репарація ушкоджень ДНК індукованих вільними радикалами кисню: Значення для розуміння причин природньогостаріння і хвороб пов'язаних зі старінням.
1Маткаримов Б. Т., 2Сапарбаєв М. К.
  1. "National Laboratory Astana", Назарбаєв Університету  
    Кабанбай-батира 53, Астана, Казахстан, 010000
  2. Інститут Густава Русі
    вул. Едуарда Вальян, 114, Вільжюіф, Франція, 94805

Abstract

Аеробне клітинне дихання генерує активні форми кисню (ROS), які можуть пошкоджувати макромолекули, включаючи ліпіди, білки і ДНК. В даний час вважається, що старіння є наслідком природного і незворотного накопичення окисних ушкоджень в клітинній ДНК. В середньому приблизно в кожній клітині людини відбувається від 2000 до 8000 пошкоджень ДНК за годину або приблизно від 40000 до 200000 пошкоджень на клітку на день. Системи репарації ДНК здатні розрізняти нормальні неушкоджені і модифіковані основи ДНК. Наприклад, ДНК глікозілази специфічно розпізнають і видаляють пошкоджені основи серед безлічі нормальних непошкоджених основ при ексцизійній репарації основ (base excision repair, BER). Проте через спонтанні конверсії 5-метілцітозіна у тимін, а також помилки ДНК-полімерази під час реплікації можуть виникати помилково спарені неушкоджені основи ДНК. Щоб протидіяти мутаціям що виникають через помилкове спарювання основ і становлять загрозу стабільності геному, клітини в процесі еволюції розвинули спеціальні системи репарації ДНК, які можуть видаляти помилково вбудовані або неспарені нормальні основи у непошкодженому ланцюга ДНК в дуплексі. Шлях репарації BER за участю Аденін- і Тимин-ДНК-глікозілаз (MutY / MUTYH і TDG / MBD4, відповідно) специфічних до неспареним підставах в дуплексі ДНК, а також шлях репарації помилково спарених некомплементарни пар основ (mismatch repair, MMR) можуть розпізнавати і видаляти нормальні неушкоджені основи в помилково спарених парах основ в дуплексах ДНК. Парадоксально, але при певних обставинах в клітинах дефіцитних по репарації ДНК, бактеріальна ДНК глікозілаза MutY і людська ДНК глікозілаза TDG можуть діяти аберрантним шляхом: MutY і TDG видаляють помилково спарені аденін і тимін які знаходяться навпроти 8-оксогуаніна і пошкодженого аденіну, відповідно. Ці аберрантние ферментні реакції призводять або до мутацій, або до марної циклічної репарації ДНК, що вказує на те, що шляхи репарації ДНК, які спрямовані на неушкоджену ланцюг ДНК в дуплексі, можуть діяти аномально і приводити до нестабільності генома в присутності нерепарованних пошкоджень ДНК. Описано факти, які свідчать що крім накопичення окисного пошкодження ДНК в клітинах, аберрантна репарація ДНК може також сприяти таким захворюванням як рак, дегенеративні зміни в головному мозку і передчасне старіння. У цьому огляді підсумовані наявні знання про аберрантні шляхи репарації ДНК окисних пошкоджень ДНК і їхня можлива роль у старінні.
Keywords: окисне пошкодження ДНК, кристалічна структура, екзиційна репарація основ, , АР ендонуклеаза
Повний текст: (PDF, англійською)

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