After cardiac arrest, organ damage consequent to ischemia‐reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in‐ or out‐of‐hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S‐transferase while decreasing the activity of serum paraoxonase‐1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.

We propose that oxidative damage may play a role in the pathogenesis of iron deficiency anaemia (IDA). Participants were selected from Basic Attention Ambulatory from North of Rio Grande do Sul, Brazil. All subjects were older than 65 years — 17 patients with IDA and primary hypertension and 18 patients with primary hypertension (control group) were included in the present study. We measured antioxidant defenses including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and total glutathione (GSH) by spectrophotometric assays. We also determined protein oxidative damage in haemolysate and plasma by carbonyl assay. We characterized the lipid peroxidation by malondialdehyde (MDA) accumulation. The results show that IDA patients had significantly higher CAT and SOD levels than controls. GPx activity was not different between the groups. Oxidative protein damage was noted in the plasma but not in the haemolysate. A significantly enhanced production of MDA was observed in the serum of IDA patients, as an indication of increased level of auto-oxidizable lipids under oxidative stress. These results support the idea that patients with IDA are subjected to chronic oxidative stress. Therefore it is important that IDA in older persons receives adequate attention in clinical practice and is not considered simply a part of normal aging.

INTRODUCTION: The capacity to overcome the oxidative stress imposed by phagocytes seems to be critical for Candida species to cause invasive candidiasis. METHODS: To better characterize the oxidative stress response (OSR) of 8 clinically relevant Candida sp., glutathione, a vital component of the intracellular redox balance, was measured using the 5,5'-dithiobis-(2-nitrobenzoic acid (DTNB)-glutathione disulfide (GSSG) reductase reconversion method; the total antioxidant capacity (TAC) was measured using a modified method based on the decolorization of the 2,2'-azinobis-(3-ethylbenzothiazoline-6-sulfonic) acid radical cation (ABTS*+). Both methods were used with cellular Candida sp. extracts treated or not with hydrogen peroxide (0.5 mM). RESULTS: Oxidative stress induced by hydrogen peroxide clearly reduced intracellular glutathione levels. This depletion was stronger in Candida albicans and the levels of glutathione in untreated cells were also higher in this species. The TAC demonstrated intra-specific variation. CONCLUSIONS: Glutathione levels did not correlate with the measured TAC values, despite this being the most important non-enzymatic intracellular antioxidant molecule. The results indicate that the isolated measurement of TAC does not give a clear picture of the ability of a given Candida sp. to respond to oxidative stress.