Dietary n-3 polyunsaturated fatty acids revert renal responses induced by a combination of 2 protocols that increase the amounts of advanced glycation end product in rats.

Renal dysfunction is a severe complication that is caused by diabetes mellitus. Many factors associate the progression of this complication with high levels of proinflammatory and pro-oxidant substances, such as advanced glycation end products (AGEs), which form a heterogeneous group of compounds that can accumulate in tissues such as retinas, joints, and kidneys. The hypothesis of this study is that n-3 polyunsaturated fatty acids (n-3 PUFAs) have a nephroprotective effect on rats after exposing them to a combination of 2 protocols that increase the AGE amounts: a high-fat diet enriched with AGEs and a diabetes rat model. Adult Wistar rats were divided into 6 groups that received the following diets for 4 weeks: (1) control group; 2) HAGE: high AGE fat-containing diet group; (3) HAGE + n-3: high AGE fat-containing diet plus n-3 PUFAs group; (4) diabetic group; (5) Db + HAGE: high AGE fat-containing diet diabetic group; and (6) Db + HAGE + n-3: high AGE fat-containing diet plus n-3 PUFAs diabetic group. Diabetes mellitus was induced by an intraperitoneal injection of alloxan (150 mg kg(-1)). In diabetic and nondiabetic rats, the high HAGE fat-containing diet increased the serum creatinine, tumor necrosis factor-α, thiobarbituric acid reactive substances, and reactive oxygen species levels, as well as the superoxide dismutase/catalase + glutathione peroxidase ratio and the superoxide dismutase 2 and receptor for advanced glycation end products immunocontent of the kidneys. n-3 Polyunsaturated fatty acids attenuated these alterations and influenced the receptor for advanced glycation end products/oxidative stress/tumor necrosis factor-α axis. In summary, this study showed that the extrinsic AGE pathway (HAGE diet) had a greater effect on renal metabolism than the intrinsic AGE pathway (diabetes induction) and that n-3 PUFAs appear to prevent renal dysfunction via antioxidant and anti-inflammatory pathways.

Similarities in serum oxidative stress markers and inflammatory cytokines in patients with overt schizophrenia at early and late stages of chronicity.

Schizophrenia (SZ) is a debilitating neurodevelopmental disorder that strikes at a critical period of a young person's life. Its pathophysiology could be the result of deregulation of synaptic plasticity, with downstream alterations of inflammatory immune processes regulate by cytokines, impaired antioxidant defense and increased lipid peroxidation. The aim of this study was to examine serum oxidative stress markers and inflammatory cytokines in early and late phases of chronic SZ. Twenty-two patients at early stage (within first 10 years of a psychotic episode), 39 at late stage (minimum 10 years after diagnosis of SZ) and their respective matched controls were included. Each subject had 5 ml blood samples collected by venipuncture to examined thiobarbituric acid-reactive substances (TBARS), total reactive antioxidant potential (TRAP), protein carbonyl content (PCC), Interleukins 6 and 10 (IL-6, IL-10) and tumor necrosis factor alpha (TNF-alpha). TBARS, IL-6 and PCC levels were significantly higher in patients with SZ at early and late stages than in controls. There were no differences for TRAP and TNF-alpha levels in patients with SZ at early and late stages than in controls. IL-10 levels were decreased in patients at late stage and a decrease trend in early stage was found. Results provided evidence consistent with comparable biological markers across chronic SZ. The concept of biochemical staging proposed by others for bipolar disorder is not seen in this cohort of patients with SZ, at least for cytokines and oxidative stress markers. Our findings reinforce the need of assessment of individuals in ultra high risk to develop psychosis and first-episode population.