**7.1 Hydroxyl radicals**

*Antioxidants*

against invading pathogens [99].

**5.3 Free radical cause lipid peroxidation**

nescence and aging-related disorders [102].

**6.1 Free radical cause peroxynitrites**

and vascular dysfunction [107].

**6.2 Free radical cause nitric oxide**

**6. Renal diseases**

platelet activation and hemostasis, and significantly contribute to the immune response [96]. Elevated reactive oxygen and nitrogen species are reduced levels of glutathione with chronic systemic inflammation with elevated levels of pro-inflammatory cytokines [97]. The ONOO▬ could be modified by the histone proteins that lead to formation of oxidatively nitrated histones in the initiation and progression of autoimmune inflammatory diseases [98]. Peroxynitrite represents both a pathophysiologically relevant endogenous cytotoxin and a cytotoxic effector against invading pathogens [99]. Being a mediator of protein oxidation and nitration, lipid peroxidation, mitochondrial dysfunction, and cell death, peroxynitrite represents both a pathophysiologically relevant endogenous cytotoxin and a cytotoxic effector

Plasma malondialdehyde and glutathione levels have been used as a determinate

Ischemia-reperfusion injury showed decreased levels of 3-nitrotyrosine-protein adducts. The iNOS-generated NO mediates damage in I-R injury possibly through ONOO▬ formation [103]. Patients with chronic renal failure (CRF) showed decreased endothelium-dependent vasodilatation to acetylcholine, have increased markers of oxidative stress, and diminished antioxidant activity [104]. ONOO▬ could induce entire mitochondrial protein nitration, responsible for the damage of renal mitochondria in diabetes [105]. Nitrosative stress is involved in cisplatininduced nephrotoxicity in rats through peroxynitrite-induced nephrotoxicity and protein nitration [106]. Renal hypoxia and ischemia promotes the formation of reactive oxygen species (ROS) such as superoxide radical anions, peroxides, and hydroxyl radicals, that can oxidatively damage biomolecules and membranes, and affect organelle function and induce renal tubule cell injury, inflammation,

The rate of whole body NO synthesis was increased in the end stage renal disease (ESRD) patients [108]. In several animal models of renal disease, the increase in NO synthesis is associated with reduced degree of glomerulosclerosis, infiltration of the kidney by invading macrophages [109]. The relations between endothelial and inducible nitric oxide synthases are perturbed in renal ischemia primarily as a result of endothelial dysfunction [110]. The nitric oxide is highly reactive and exerts its chronic effects only at high concentrations which are responsible for the complications of dialysis of patients with chronic kidney disease [111]. Patients with chronic kidney disease (CKD) have been found the decreased levels in all stages of CKD [112]. Intracellular nitric oxide (iNO) substantially increased the risk of renal

of oxidative status in the chronic immunological disorders; systemic lupus erythematosus (SLE) is a complex [100]. 4-Oxo-2-nonenal (ONE) is a highly reactive aldehyde originating from the peroxidation of polyunsaturated fatty acids involved in the pathogenesis of autoimmune disorders [101]. The product of lipid peroxidation is 4-hydroxynonenal (HNE) that acts as specific marker of immunose-

**376**

It is the most reactive of the free radical molecules. It damages cell membranes and lipoproteins by lipid peroxidation. Damage to lipoproteins in low density lipoprotein plays an important role in atherosclerosis. ∙OH is formed by radiolysis of water and by reaction of H2O2 with ferrous (Fe2+) ions; the latter process is termed as Fenton reaction [116, 117]. The reactive oxygen species, hydroxyl (∙OH) radical is one of the potential inducers of DNA damage. A variety of adducts are formed on reaction of ∙OH radical with DNA. The ∙OH radical can attack purine and pyrimidine bases to form ∙OH radical adducts, which are both oxidizing and reducing in nature which in turn can induce base modifications and sometimes release of bases. Some of the important base modifications include 8-hydroxydeoxyguanosine (8-OHdG), 8 (or 4-,5-)-hydroxyadenine, thymine peroxide, thymine glycols, and 5-(hydroxymethyl) uracil [118].
