Nội dung được dịch bởi AI, chỉ mang tính chất tham khảo
Một khuôn mẫu mới cho sự sinh ra các loài phản ứng được xúc tác bởi XOR trong nội mô
Tóm tắt
Một loạt bệnh lý mạch máu liên quan đến viêm, trạng thái thiếu oxy và tỷ lệ tạo ra các loài phản ứng gia tăng. Một nguồn chính của các loài phản ứng này là enzym phân giải purine xanthine oxidoreductase (XOR) khi nhiều báo cáo trong 30 năm qua đã chứng minh rằng sự ức chế XOR có tác dụng tích cực. Mặc dù có sự liên hệ lâu dài giữa hoạt động XOR mạch máu gia tăng và các kết quả lâm sàng tiêu cực, các báo cáo gần đây tiết lộ một khuôn mẫu mới, nơi mà hoạt động enzym của XOR trung gian cho các kết quả có lợi bằng cách xúc tác phản ứng khử nitrit (NO2−) thành nitric oxide (NO) khi nồng độ NO2− và/hoặc nitrate (NO3−) tăng cường thông qua chế độ ăn uống hoặc phương tiện dược lý. Những quan sát này dường như trái ngược với nhiều báo cáo về kết quả cải thiện trong các mô hình tương tự khi ức chế XOR trong trường hợp không có điều trị NO2−, khẳng định sự cần thiết phải hiểu rõ hơn về các cơ chế liên quan đến danh tính sản phẩm của XOR. Để thiết lập các điều kiện vi mô cần thiết cho sản xuất oxy hóa và NO được xúc tác bởi XOR trong cơ thể sống, bài review này đánh giá tác động của pH, áp suất O2, tương tác enzyme–nội mô, nồng độ chất nền và sự khác biệt xúc tác giữa xanthine oxidase (XO) và xanthine dehydrogenase (XDH). Như vậy, nó tiết lộ thông tin quan trọng cần thiết để phân biệt liệu việc theo đuổi bổ sung NO2− sẽ mang lại lợi ích lớn hơn so với các chiến lược ức chế và do đó nâng cao hiệu quả của các phương pháp hiện tại trong điều trị bệnh lý mạch máu.
Từ khóa
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