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Ferroptosis, a novel programmed cell death characterized by intracellular accumulation of lipid peroxides, has played an important role in a wide range of diseases. Acute lung injury is a critical illness caused by several reasons, and the mortality rate is high. With increasing research on the mechanism of acute lung injury, more evidence has shown that ferroptosis played an important role in the pathogenesis of acute lung injury. In this paper, we sorted the previous studies related to ferroptosis and found that all acute lung injury induced by ischemia-reperfusion, sepsis, radiation, drowning and oleic acid were involved in ferroptosis. We hope to provide a promising theoreticalbasis for the future diagnosis and treatment of acute lung injury by summarizing the mechanism of ferroptosis and its role in the pathogenesis of acute lung injury.

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Background and objective The relationship between antioxidants and tumor was gradually paid attention. The changes of activities and the levels of expression mRNA and protein of oxidants and antioxidants, were evaluated in 113 lung tumor and 64 tumor-free lung tissues collected between the years 2006 and 2007 from 113individuals with surgically resectable lung cancer in order to understand the mechanism of the onset and development of lung cancer. Methods The activities of TSOD, MnSOD, CuZnSOD, GPx, H2O2 and MDA were determined by chromometry.MnSOD, CuZnSOD mRNA and protein expression levels were evaluated by Reverse transcription polymerase chain reaction and Western Blot analysis in tumor tissues, as well as corresponding control tissues. Results Comparing with the levels of these indexes in the tumor-free tissues, the activities of TSOD, CuZnSOD, GPx were higher, H2O2 and MDA were lower in the tumor tissues (P

Objective: To investigate the changes of aldehyde dehydrogenase 2 (ALDH2) expression in H 2 O 2 inducedcardiomyocytes oxidative stress injury., Methods: Cultured H9C2 cardiomyocytes were exposed to H 2 O 2 -inducedoxidative stress and the effects of the ALDH2 agonist Alda-1 and ALDH2 inhibitor Daidzin were tested on the stress level ofthe exposed cells. MTT colorimetric assay was used to assess the cell viability after the treatments. The oxidative stress level inthe myocardial cells was detected using DHE fluorescence staining, and the activity and protein level of ALDH2 were detectedwith spectrophotometry and Western blotting., Results: Compared with normal control cells, Alda-1 treatment did notsignificantly affect the cell viability, oxidative stress level, or ALDH2 activity and protein level. H 2 O 2 exposure significantlylowered the cell activity and ALDH2 activity and protein expression and increased the oxidative stress level; Alda-1 treatmentobvious antagonized the effects of H 2 O 2 . Blocking ALDH2 with Daidzin produced similar effects to H 2 O 2 exposure on theviability, oxidative stress level, and ALDH2 activity and expression in the myocardial cells., Conclusions: H 2 O 2 exposure lowersthe activity and reduces the protein expression of ALDH2 in cardiomyocyte H9C2 cells, and activation of ALDH2 can alleviateH 2 O 2 -induced oxidative stress in the cells.

Objective: To investigate the effects of resveratrol (RES) on apoptosis of human periodontal ligament cells (HPLC)., Methods: HPLC were subjected to oxidative injury induced by H2O2 for 24 h after pretreatment with different concentration of RES. HPLC were then divided into the control, model, vector, RES 1, 10, 30, 50 micromol/L treatment group. The viability of the HPLC was determined by methyl thiazolyl tetrazolium (MTT) method. Lactate dehydrogenase (LDH) rate and malondialdehyde (MDA) in the culture medium, superoxide dismutase (SOD) in the HPLC homogenate were evaluated by spectrophotometry. The apoptotic HPLC was detected by flow cytometry (FCM) and calculated by relative apoptosis rate. Bax and Bcl-2 protein levels were detected by Western blotting., Results: RES increased the cell survival rate after H2O2 injury. The survival rate of RES 30 micromol/L group was (86.1 +/- 4.1)% and the model group was (54.6 +/- 4.0)%, which was significantly different between the two groups (P < 0.01). The LDH leakage rate and MDA content of the RES 30 micromol/L group were (32.6 +/- 2.0)% and (1.70 +/- 0.21) micromol/L, which were significantly different with that in the model group (P < 0.01). At the same time RES could remarkably restore the vitality of SOD in the HPLC. RES increased Bcl-2 and reduced the expression of Bax protein. The apoptosis rate of the RES 30 micromol/L group and model group was (14.84 +/- 1.36)% and (64.37 +/- 2.34)%, respectively (P < 0.01). The protective effect of RES on the cell apoptosis was in a dose-dependent manner, reaching peak at a concentration of 30 micromol/L (P < 0.01)., Conclusions: RES reduced oxidative stress and apoptosis in an experimental HPLC injury model induced by H2O2. RES plays a key role in the HPLC protection against oxidative injury.

Space flight is associated with an increase of peroxidative damage after returning to 1 g. The effect is more pronounced after long-duration space flight and can even last for several weeks after landing. In humans there is increased lipid peroxidation in erythrocyte membranes, reduced blood antioxidants, and increased urinary excretion of 8-iso-prostaglandin F2alpha, and 8-oxo-7, 8 dihydro-2 deoxyguanosine. Isoprostane 8-iso-prostaglandin F2alpha and 8-oxo-7, 8 dihydro-2 deoxyguanosine are markers for oxidative damage to lipids and DNA, respectively. The changes are attributed to a combination of energy deficiency that occurs during flight and substrate competition for amino acids occurring between repleted muscle and other tissues during the recovery phase. The observations in humans have been complemented by studies in rodents, which showed increased production of lipid peroxidation products and decreased antioxidant enzyme activity afterflight. The changes in rodents were attributed to the stress associated with re-entry into Earth's gravity. Reducing the imbalance between the production of endogenous oxidant defenses and oxidant production by increasing the supply antioxidants in diet may lessen the severity of the postflight increase in oxidative stress.

The feasible methods for oxidation and removal of arsenite[As(III)] from dispersed drinking water were based on the removal of arsenate[As(V)] by ferric sulfate. The results showed that the spotaneous oxidation of As(III) to As(V) was very slow and could not be enhanced by aerating for 24 h. The removal rate of As(III) could reach that of As(V) when pre-aerating water samples with ozone for 60 s, putting 7.5 ml/L hydrogen peroxide solution, adding 2.5 mg/L javelle water (sodium hypochlorite) or 15 mg/L bleaching powder(numerated by chlorine). The oxidation by using javelle water was rather stable when samples were varied in pH value, hardness, initial concentration of As(III) and As(III)/As(V) ratio. The effective oxidation could be reached with 1.25 mg/L javelle water when the initial concentration of As(III) was < or = 0.8 mg/L. Moreover, the field study also confirmed the oxidation effect of javelle water. It is suggested that javelle water is an effective, economic and technologic feasible oxidationagent for removing arsenite from dispersed drinking water.