Rheumatoid arthritis and oxidative

Rheumatoid arthritis and oxidative stress
Rheumatoid arthritis is an autoimmune disease characterized
by chronic inflammation of the joints and tissue
around the joints with infiltration of macrophages and activated
T cells (4, 25, 26). The pathogenesis of this disease
is due to the generation of ROS and RNS at the site of inflammation.
Oxidative damage and inflammation in various
rheumatic diseases were proved by increased levels
of isoprostanes and prostaglandins in serum and synovial
fluid compared to controls (26).
Nephropathy and oxidative stress
Oxidative stress plays a role in a variety of renal diseases
such as glomerulonephritis and tubulointerstitial nephritis,
chronic renal failure, proteinuria, uremia (5, 27).
The nephrotoxicity of certain drugs such as cyclosporine,
tacrolimus (FK506), gentamycin, bleomycin, vinblastine,
is mainly due to oxidative stress via lipid peroxidation (27-
30). Heavy metals (Cd, Hg, Pb, As) and transition metals
(Fe, Cu, Co, Cr)-induced different forms of nephropathy
and carcinogenicity are strong free radical inducers in the
body (11, 12).
Ocular disease and oxidative stress
Oxidative stress is implicated in age-related macular
degeneration and cataracts by altering various cell types in
the eye either photochemically or nonphotochemically (31).
Under the action of free radicals, the crystalline proteins
in the lens can cross-link and aggregate, leading to the formation
of cataracts (32). In the retina, long-term exposure
to radiation can inhibit mitosis in the retinal pigment epithelium
and choroids, damage the photoreceptor outer segments,
and has been associated with lipid peroxidation (33).
Fetus and oxidative stress
Oxidative stress is involved in many mechanisms in the
development of fetal growth restriction and pre-eclampsia
in prenatal medicine (34-37). Some reports indicate that
blood levels of lipid peroxidation products (F2-isoprostanes,
MDA) are elevated in pre-eclamptic pregnancy and
intra-uterine growth retardation and it has been suggested
that ROS/RNS play a role in the etiology of these diseases
(35-37). In pregnancies complicated by pre-eclampsia, increased
expression of NADPH oxidase 1 and 5 isoforms
which are the major enzymatic sources of superoxide in
the placenta is seen (37).
Finally, Figure 1 summarizes oxidative stress-induced
diseases in humans.
ANTIOXIDANTS AND HEALTH MAINTENANCE
The body has several mechanisms to counteract oxidative
stress by producing antioxidants, either naturally generated
in situ (endogenous antioxidants), or externally supplied
through foods (exogenous antioxidants). The roles of
antioxidants are to neutralize the excess of free radicals, to
protect the cells against their toxic effects and to contribute
to disease prevention.

Results (English) 2:

类风湿性关节炎和氧化应激
类风湿性关节炎是一种自身免疫性疾病的特点
的关节和关节周围组织
与巨噬细胞浸润的慢性炎症和T细胞活化
（4，25，26）。本病的发病机制是由于
在炎症部位的ROS和RNS的产生。
各种
氧化损伤和炎症风湿性疾病是由
水平升高血清和关节液
异前列腺素和前列腺素的对照组比较，证明了（26）。
肾病和氧化应激
氧化应激是多种肾脏疾病的作用
如肾小球肾炎、肾小管间质性肾炎，慢性肾功能衰竭
，蛋白尿，尿毒症（5，27）。
某些药物如环孢素肾毒性，
他克莫司（FK506），庆大霉素，长春新碱，博莱霉素，
主要是由于氧化应激通过脂质过氧化（27
30）。重金属（镉，汞，铅，如）和过渡金属（Fe，Cu
，Co，Cr）诱导的不同形式的肾病
和致癌性在
身体自由基诱导剂（11，12）。
眼部疾病和氧化应激
氧化应激与年龄相关的黄斑变性、白内障
通过改变不同的细胞类型中的
眼睛光化学或nonphotochemically（31）。
自由基的作用下，在镜头中的蛋白质晶体
可交联和聚合，导致白内障的形成
（32）。在视网膜中，长期暴露
辐射能抑制视网膜色素上皮和脉络膜损伤
分裂，光感受器外段，
已与脂质过氧化（33）。
胎儿和氧化应激
氧化应激在胎儿生长受限和先兆子痫
产前医学
发展中的许多机制（34-37）。一些报告表明，
血液水平的脂质过氧化产物（F2-异前列烷，
MDA）在妊娠先兆子痫和
宫内发育迟缓升高，它已被建议
，ROS / RNS发挥作用，这些疾病的病因
（35-37）。妊娠合并先兆子痫，NADPH氧化酶的亚型1和5
是超
主要来源
酶表达增加胎盘是（37）。
最后，图1总结了在人类疾病的氧化应激
。
抗氧化剂和健康维护
身体对抗氧化应激的
生产抗氧化剂的几种机制，无论是自然产生的
原位（内源性抗氧化剂），或通过外部提供的
食品（抗氧化剂）。
的角色抗氧化剂是中和自由基的过量，对
保护细胞免受毒性效应和贡献
疾病预防。