Ferroptosis regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer

BACKGROUND Gastric cancer is one of the most common malignant tumors in the world,and its occurrence and development involve complex biological processes.Iron death,as a new cell death mode,has attracted wide attention in recent years.However,the regulatory mechanism of iron death in gastric cancer and its effect on lipid peroxidation metabolism remain unclear.AIM To explore the role of iron death in the development of gastric cancer,reveal its relationship with lipid peroxidation,and provide a new theoretical basis for revealing the molecular mechanism of the occurrence and development of gastric cancer.METHODS The process of iron death in gastric cancer cells was simulated by cell culture model,and the occurrence of iron death was detected by fluorescence microscopy and flow cytometry.The changes of gene expression related to iron death and lipid peroxidation metabolism were analyzed by high-throughput sequencing technology.In addition,a mouse model of gastric cancer was established,and the role of iron death in vivo was studied by histology and immunohistochemistry,and the level of lipid peroxidation was detected.These methods comprehensively and deeply reveal the regulatory mechanism of iron death on lipid peroxidation metabolism in the occurrence and development of gastric cancer.RESULTS Iron death was significantly activated in gastric cancer cells,and at the same time,associated lipid peroxidation levels increased significantly.Through high-throughput sequencing analysis,it was found that iron death regulated the expression of several genes related to lipid metabolism.In vivo experiments demonstrated that increased iron death in gastric cancer mice was accompanied by a significant increase in lipid peroxidation.CONCLUSION This study confirmed the important role of iron death in regulating lipid peroxidation metabolism in the occurrence and development of gastric cancer.The activation of iron death significantly increased lipid peroxidation levels,revealing its regulatory mechanism inside the cell.

Research progress of ferroptosis regulating lipid peroxidation and metabolism in occurrence and development of primary liver cancer

As a highly aggressive tumor,the pathophysiological mechanism of primary liver cancer has attracted much attention.In recent years,factors such as ferroptosis regulation,lipid peroxidation and metabolic abnormalities have emerged in the study of liver cancer,providing a new perspective for understanding the development of liver cancer.Ferroptosis regulation,lipid peroxidation and metabolic abnormalities play important roles in the occurrence and development of liver cancer.The regulation of ferroptosis is involved in apoptosis and necrosis,affecting cell survival and death.Lipid peroxidation promotes oxidative damage and promotes the invasion of liver cancer cells.Metabolic abnormalities,especially the disorders of glucose and lipid metabolism,directly affect the proliferation and growth of liver cancer cells.Studies of ferroptosis regulation and lipid peroxidation may help to discover new therapeutic targets and improve therapeutic outcomes.The understanding of metabolic abnormalities can provide new ideas for the prevention of liver cancer,and reduce the risk of disease by adjusting the metabolic process.This review focuses on the key roles of ferroptosis regulation,lipid peroxidation and metabolic abnormalities in this process.

Vicious cycle of lipid peroxidation and iron accumulation in neurodegeneration

Lipid peroxidation and iron accumulation are closely associated with neurodegenerative diseases,such as Alzheimer’s,Parkinson’s,and Huntington’s diseases,or neurodegeneration with brain iron accumulation disorders.Mitochondrial dysfunction,lipofuscin accumulation,autophagy disruption,and ferroptosis have been implicated as the critical pathomechanisms of lipid peroxidation and iron accumulation in these disorders.Currently,the connection between lipid peroxidation and iron accumulation and the initial cause or consequence in neurodegeneration processes is unclear.In this review,we have compiled the known mechanisms by which lipid peroxidation triggers iron accumulation and lipofuscin formation,and the effect of iron overload on lipid peroxidation and cellular function.The vicious cycle established between both pathological alterations may lead to the development of neurodegeneration.Therefore,the investigation of these mechanisms is essential for exploring therapeutic strategies to restrict neurodegeneration.In addition,we discuss the interplay between lipid peroxidation and iron accumulation in neurodegeneration,particularly in PLA2G6-associated neurodegeneration,a rare neurodegenerative disease with autosomal recessive inheritance,which belongs to the group of neurodegeneration with brain iron accumulation disorders.

Effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7S)and glycinin(11S)

This study aimed to analyze the effect of lipid peroxidation on the allergenicity and functional properties of soybeanβ-conglycinin(7 S)and glycinin(11 S).Oxidation complexes were determined using the lipid peroxidation method.Functional properties were analyzed based on emulsifying and foaming properties.The potential allergenicity was evaluated by in vitro and in vivo methods.The results found that oxidation altered structures of the proteins and resulted in the formation of cross-linked protein polymers.The emulsion and foaming properties of the proteins were improved after oxidation.The IgE-binding capacity of 7 S and11 S reduced after oxidation.KU812 cell assays showed that both histamine and IL-4 release decreased after oxidation treatment.A mouse model showed that oxidation reduced the IgE,IgG,and IgG1 levels,as well as reduced histamine and mMCP-1 release in serum,which might suppress the allergic reaction.In conclusion,the lipid peroxidation treatment likely causes changes to the functional properties of soybean,decreasing the potential allergenicity of 7 S and 11 S.

Investigation of heavy metals and lipid peroxidation level in the muscles of Clarias gariepinus from IBI,Gindin-Dorowa and D onga community rivers in Taraba State,Nigeria

Heavy metals have harmful effects on human health,and exposure to these metals has been increased by industrial and anthropogenic activities and modern industrialization.Heavy metals content of the liver tissues was determine d using Atomic Absorption Spectrophotometer method,while lipid peroxidation was carried out.Heavy metals analyzed include;lead(Pb),cadmium(Cd),zinc(Zn),Arsenic(As),and Mercury(Hg).The findings revealed that the heavy metal Zinc(Zn)has high concentrations in the muscles of the fish species,the concentration of this heavy metal Zinc is high in River Gindin Dorowa th a n in River Ibi and River Donga shows less concentration of this heavy metal though it’s above WHO permissible limits.Results revealed that only Zn and Cd were present in the muscle from the three rivers.Pb was found only in the liver from Gindin-Dorowa at the concentration of 0.017 mg/kg,which is not significant(P<0.05)when compared with other locations,while Hg and As were absent in all the muscle samples.The highest concentration of Zn was found in the muscle sample from Gindin-Dorowa(7.450 mg/kg)followed by Ibi(6.16 mg/kg)and the least being Donga(4.365 mg/kg)which are significantly(P<0.05)different from one another.However,there was no significant(P<0.05)difference among the Cd composition of muscle from Gindin-Dorowa(0.025 mg/kg),Donga(0.024 mg/kg)and Ibi(0.015 mg/kg),respectively.The TBA was found in the hepatic tissue sample from Gidin-Dorowa,which has the highest Zn,Cd and no Pb content,followed by Ibi and then the Donga sample.This suggests that there is a positive relationship between heavy metals and the effect of TBA on the hepatic tissues,justifying the fact that heavy metals affect the hepatic tissues of fish,while on the cerebral tissue.In conclusion,it revealed that there is a negative relation between heavy metals and the effect of TBA on the cerebral tissues to protect or save aquatic habitat s of fish quality and aquatic life.

Potential role and therapeutic implications of glutathione peroxidase 4 in the treatment of Alzheimer's disease

Alzheimer's disease is an age-related neurodegenerative disorder with a complex and incompletely understood pathogenesis. Despite extensive research, a cure for Alzheimer's disease has not yet been found. Oxidative stress mediates excessive oxidative responses, and its involvement in Alzheimer's disease pathogenesis as a primary or secondary pathological event is widely accepted. As a member of the selenium-containing antioxidant enzyme family, glutathione peroxidase 4 reduces esterified phospholipid hydroperoxides to maintain cellular redox homeostasis. With the discovery of ferroptosis, the central role of glutathione peroxidase 4 in anti-lipid peroxidation in several diseases, including Alzheimer's disease, has received widespread attention. Increasing evidence suggests that glutathione peroxidase 4 expression is inhibited in the Alzheimer's disease brain, resulting in oxidative stress, inflammation, ferroptosis, and apoptosis, which are closely associated with pathological damage in Alzheimer's disease. Several therapeutic approaches, such as small molecule drugs, natural plant products, and non-pharmacological treatments, ameliorate pathological damage and cognitive function in Alzheimer's disease by promoting glutathione peroxidase 4 expression and enhancing glutathione peroxidase 4 activity. Therefore, glutathione peroxidase 4 upregulation may be a promising strategy for the treatment of Alzheimer's disease. This review provides an overview of the gene structure, biological functions, and regulatory mechanisms of glutathione peroxidase 4, a discussion on the important role of glutathione peroxidase 4 in pathological events closely related to Alzheimer's disease, and a summary of the advances in small-molecule drugs, natural plant products, and non-pharmacological therapies targeting glutathione peroxidase 4 for the treatment of Alzheimer's disease. Most prior studies on this subject used animal models, and relevant clinical studies are lacking. Future clinical trials are required to validate the therapeutic effects of strategies targeting glutathione peroxidase 4 in the treatment of Alzheimer's disease.

Mechanisms of Inhibitory Effects of Breviscapine on Lipid Peroxidation in Rat Brain Mitochondria

本文研究了灯盏花素抑制脂质过氧化的作用机制。大鼠脑线粒体脂质过氧化物用硫代巴比妥酸比色法测定。灯盏花素与铁的螯合活性用差示光谱法测定。黄嘌呤黄嘌呤氧化酶（ＸａｎＸＯ）体系产生的超氧阴离子自由基（Ｏ２）及ＦｅＳＯ４Ｈ２Ｏ２体系产生的羟自由基（·ＯＨ）用比色法测定。结果表明：灯盏花素能有效地抑制ＸａｎＸＯ和ＦｅＳＯ４Ｈ２Ｏ２诱导的脑线粒体脂质过氧化反应，其ＩＣ５０分别为９３０１和６２１８μｍｏｌ·Ｌ－１。灯盏花素也能清除ＸａｎＸＯ体系产生的Ｏ２和ＦｅＳＯ４Ｈ２Ｏ２体系产生的·ＯＨ，其ＩＣ５０分别为３２６３和２０２２μｍｏｌ·Ｌ－１。灯盏花素还具有螯合Ｆｅ２＋的活性。由此可见，灯盏花素是在氧自由基与线粒体膜的反应中（１）·ＯＨ的形成（通过与Ｆｅ２＋螯合）（２）脂质过氧化的启动（通过清除Ｏ２和·ＯＨ）两个环节抑制脂质过氧化反应的。

Modulatory effect of pineapple peel extract on lipid peroxidation,catalase activity and hepatic biomarker levels in blood plasma of alcoholinduced oxidative stressed rats

Objective:To investigate the ability of the methanolic extract of pineapple peel to modulate alcohol-induced lipid peroxidation,changes in catalase activities and hepatic biochemical marker levels in blood plasma.Methods:Oxidative stress was induced by oral administration of ethanol(20%w/v) at a dosage of 5 niL/kg bw in rats.After 28 days of treatment,the rats were fasted overnight and sacrificed by cervical dislocation.Blood was collected with a 2 mL syringe by cardiac puncture and was centrifuged at 3000 rpm for 10 min.The plasma was analyzed to evaluate malondialdehyde(MDA),catalase activity,aspartate aminotransferase(AST),alkaline phosphatase(ALP) and alanine aminotransferase(ALT) concentrations.Results:Administration of alcohol caused a drastic increase(87.74%) in MDA level compared with the control.Pineapple peel extract significantly reduced the MDA level by 60.16%at 2.S mL/kg bw.Rats fed alcohol only had the highest catalase activity,treatment with pineapple peel extract at 2.5 mL/kg bw however, reduced the activity.Increased AST,ALP and ALT activities were observed in rats fed alcohol only respectively,treatment with pineapple peel extract drastically reduced their activities. Conclusions:The positive modulation of lipid peroxidation,catalase activities as well as hepatic biomarker levels of blood plasma by the methanolic extract of pineapple peels under alcoholinduced oxidative stress is an indication of its protective ability in the management of alcoholinduced toxicity.

Effects of melatonin on lipid peroxidation and antioxidant enzymes in streptozotocin-induced diabetic rat testis

Aim： To examine the effects of melatonin treatment on lipid peroxidation （LPO） and the activities of antioxidant enzymes in the testicular tissue of streptozotocin （STZ）-induced diabetic rats. Methods： Twenty-six male rats were randomly divided into three groups as follows： group Ⅰ, control, non-diabetic rats （n = 9）; group Ⅱ, STZ-induced, untreated diabetic rats （n = 8）; group Ⅲ, STZ-induced, melatonin-treated （dose of 10 mg/kg·day） diabetic rats （n = 9）. Following 8-week melatonin treatment, all rats were anaesthetized and then were killed to remove testes from the scrotum. Results： As compared to group Ⅰ, in rat testicular tissues of grouap Ⅱ, increased levels of malondialdehyde （MDA） （P 〈 0.01） and superoxide dismutase （SOD） （P 〈 0.01） as well as, decreased levels of catalase （CAT） （P 〈 0.01） and glutathione peroxidase （GSH-Px） （P 〉 0.05） were found. In contrast, as compared to group Ⅱ, in rat testicular tissues of group Ⅲ, levels of MDA decreased （but this decrease was not significant, P 〉 0.05） and SOD （P 〈 0.01） as well as CAT （P 〈 0.05） increased. GSH-Px was not influenced by any of the treatment. Melatonin did not significantly affect the elevated glucose concentration of diabetic group. At the end of the study, there was no significant difference between the melatonin-treated group and the untreated group by means of body and testicular weight. Conclusion： Diabetes mellitus increases oxidative stress and melatonin inhibits lipid peroxidation and might regulate the activities of antioxidant enzymes of diabetic rat testes.

Effects of Water Stress on the Protective Enzyme Activities and Lipid Peroxidation in Roots and Leaves of Summer Maize

A systematic study was conducted to determine the effects of water stress on the activities of protective enzymes and lipid peroxidation in maize. The results showed that, under water stress, the activities of superoxide dismutase （SOD）, catalase （CAT）, and peroxidase （POD） in leaves and roots increased sharply at prophase and metaphase growth stages, such as, male tetrad stage, but then declined towards the physiological maturity. The protective enzyme activities in roots were lower than those in leaves. The content of malondialdehyde （MDA） increased according to the severity of water stress. The content of MDA in roots was lower than that in leaves. The activities of protective enzymes and lipid peroxidation in roots were positively related to that in leaves with most of the correlation coefficients being significant. The content of soluble proteins in roots and leaves decreased with increasing drought stress. The ear characteristics deteriorated and the economic yields of maize decreased significantly under water stress. The main factors that caused reduction of yields were the decrease in the number of ear kernels and 100-kernel weight.

Changes of Antioxidative Enzymes and Lipid Peroxidation in Leaves and Roots of Waterlogging-Tolerant and Waterlogging-Sensitive Maize Genotypes at Seedling Stage

To better understand the physiological and biochemical mechanisms of waterlogging tolerance, waterlogging effects on lipid peroxidation and the activity of antioxidative enzymes were investigated in leaves and roots of two maize genotypes, HZ32 （waterlogging-tolerant） and K12 （waterlogging-sensitive）. Potted maize plants were waterlogged at the second leaf stage under glasshouse conditions. Leaves and roots were harvested 1 d before and 2, 4, 6, 8 and 10 d after the start of waterlogging treatment. Through comparing the activities of superoxide dismutase （SOD）, ascorbate peroxidase （APX）, glutathione reductase （GR）, catalase （CAT） and guaiacol peroxidase （POD） between waterlogging-tolerant and waterloggingsensitive genotype, we deduced that CAT was the most important H2O2 scavenging enzyme in leaves, while APX seemed to play a key role in roots. POD, APX, GR and CAT activities in conjunction with SOD seem to play an essential protective role in the O2^- and H2O2 scavenging process. Lipid peroxidation was enhanced significantly only in K12 （P 〈 0.001） and there was no difference （P 〉 0.05） in HZ32 up to 6 d after waterlogging stress. These results indicated that oxidative stress may play an important role in waterlogging-stressed maize plants and that the greater protection of HZ32 leaves and roots from waterlogging-induced oxidative damage results, at least in part, through the maintenance of increased antioxidant enzyme activity.

Antioxidant,lipid peroxidation inhibition and free radical scavenging efficacy of a diterpenoid compound sugiol isolated from Metasequoia glyptostroboides

Objective:To investigate the antioxidant enicacy of a biologically active dilerpenoid compound sugiol isolated from Metasequoia glyptostroboides(M.glyptostroboides)in various antioxidant models.Methods:An abietane type diterpenoid sugiol,isolated from ethyl acetate extract of M.glyptostroboides cones,was analyzed for its antioxidant efficacy as reducing power ability and lipid peroxidation inhibition as well as its ability to scavenge free radicals such as 1,1-diphenyl-2-picryl hydrazyl,nitric oxide,superoxide and hydroxyl radicals.Results:The sugiol showed significant and concentration-dependent antioxidant and free radical scavenging activities.Consequently,the sugiol exerted lipid peroxidation inhibitory effect by 76.3%as compared to a-tocopherol(80.13%)and butylaled hydroxyanisole(76.59%).In addition,the sugiol had significant scavenging activities of l,l-diphenyl-2-picryl hydrazyl,nitric oxide,superoxide and hydroxyl free radicals in a concentration-dependent manner by 78.83%,72.42%,72.99%and 85.04%,when compared to the standard compound ascorbic acid(81.69%,74.62%,73.00%and 73.79%)and a-tocopherol/butylated hydroxyanisole(84.09%,78.61%,74.45%and 70.02%),respectively.Conclusions:These findings justify the biological and traditional uses of M.glyptostroboides or its secondary metabolites as confirmed by its promising antioxidant efficacy.

Sperm lipid peroxidation and pro-inflammatory cytokines

Aim： To investigate if interleukin-6 （IL-6）, interleukin-8 （IL-8）, interleukin- 10 （IL-10）, interferon-gamma （IFN-γ） or tumor necrosis factor-alpha （TNF-α） are able to stimulate the level of lipid peroxidation of sperm membranes, either alone or in the presence of leukocytes. Methods： Semen samples from normozoospermic donors were prepared by density gradient. The sperms were exposed to the indicated cytokines, at physiological and infection-inflammation concentrations, in the absence or presence of leukocytes. Lipid peroxidation of the sperm membranes was determined by measuring malondialdehyde （MDA） and 4-hydroxialkenals （HAE） formation. Results： TNF-α, IL-8 and IFN-γ increased the level of sperm membrane lipid peroxidation when tested at physiological concentrations. At infectioninflammation concentrations, only IL-8 was able to produce a higher effect. When assayed in the presence of leucocytes, IL-8 and TNF-α showed a higher effect at infection-inflammation concentrations than at physiological concentrations. Finally, IL-8 showed a higher effect in the presence of leukocytes than in their absence at both physiological and infection-inflammation concentrations. TNF-α also showed a higher effect when assayed in the presence of leuko- cytes than in their absence, but only at infection-inflammation concentrations. There was no effect of IL-6 or IL-10 in any of the tested conditions. Conclusion： Several pro-inflammatory cytokines at physiological concentrations increase the level of lipid peroxidation of sperm membranes, which could be important for the sperm fecundation process. However, infection-inflammation concentrations of some cytokines, such as IL-8 and TNF-α, either alone or in the presence of leukocytes, could drive the lipid peroxidation of the spermatozoa plasma membrane to levels that can affect the sperm fertility capacity.

In vitro inhibition activity of polyphenol-rich extracts from Syzygium aromaticum(L.)Merr.& Perry(Clove)buds against carbohydrate hydrolyzing enzymes linked to type 2 diabetes and Fe^(2+)-induced lipid peroxidation in rat pancreas

Objective:To investigate and compare the inhibitor)'properties)of free and bound phenolic extracts of clove bud against carbohydrate hydrolyzing enzymes(alpha-amylase&alphaglucosidase)and Fe^(2+)-induced lipid peroxidation in rat pancreas in vitro.Methods:The free phenolics were extracted with 80%.(v/v)acetone,while bound phenolics were extracted from the alkaline and acid hydrolyzed residue with ethyl acetate.Then,the interaction of the extracts with alpha-amylase and alpha-glucosidase was subsequently assessed.Thereafter,the total phenolic contents and antioxidant activities of the extracts were determined.Results:The result revealed that both extracts inhibited alpha-amylase and alpha-glucosidase in a dose-dependent manner.However,the alpha-glucosidase inhibitory activity of the extracts were significantly(P<0.05)higher than their alpha-amylase inhibitory activity.The free phenolics(31.67 mg/g)and flavonoid(17.28 mg/g)contents were significantly(P<0.05)higher than bound phenolic(23.52 mg/g)and flavonoid(13.70 mg/g)contents.Both extracts also exhibited high antioxidant activities as typified by their high reducing power,LI diphenyl-2-picrylhydrazyl(DPPH)and 2,2-azinobis-3-ethylbenzo-thiazoline-6-sulfonate(ABTS)radical scavenging abilities,as well as inhibition of Fe^(2+)-induced lipid peroxidation in rat pancreas in vitro.Conclusions:This study provides a biochemical rationale by which clove elicits therapeutic effect on type 2 diabetes.

Lipid Peroxidation and Ultrastructural Modifications in Brain after Perinatal Exposure to Lead and/or Cadmium in Rat Pups

Objective To assess lipid peroxidation and ultrastructural modifications in rat brains following perinatal exposure to lead （Pb） and/or cadmium （Cd）. Methods Female rats were divided into four groups： control group, Pb （300 mg/L） group, Cd group （10 mg/L） and Pb＋Cd （300 mg/L, 10 mg/L） group. The compounds were delivered in the drinking water throughout pregnancy and lactation. Results The levels of compounds in blood and brain of the Pb＋Cd group were similar to those of other groups, but the effects of Pb＋Cd on pups＇ body and brain weights were higher than on other compounds. Electron microscopy revealed that Pb and Cd had effects on mitochondrial swelling, disruption and cristae loss, Nissl body dissolution, degenerated organelles and vacuoles, cytomembrane disappearance, and nuclear chromoplasm concentration. The activity of glutathione peroxidase （GSH-Px）, superoxide dismutase （SOD）, catalase （CAT）, acetylcholinesterase （ACHE） was decreased, whereas the activity of maleic dialdehyde （MDA） was increased. Conclusion Perinatal exposure to low doses of Pb and Cd can produce alterations in lipid peroxidation and ultrastructural modifications in rat brains, and exposure to both metals can result in greater damages.

Effects of Exogenous Silicon on the Activities of Antioxidant Enzymes and Lipid Peroxidation in Chilling-Stressed Cucumber Leaves

In order to increase vegetable productivity by improving environmental conditions, this article investigates the effects of exogenous silicon on the activities of major antioxidant enzymes and on lipid peroxidation under chilling stress, and it examines whether silicon-induced chilling tolerance is mediated by an increase in antioxidant activity. Cucumis sativus cv. Jinchun 4 was hydroponically cultivated to the two-leaf stage, at which point seedlings were watered with different concentrations of silicon (0, 0.1 and 1 mmol L^-1) and separately exposed to normal (25/18℃) or chilling (15/8℃) temperatures for six days under low light (100μmol m^-2 s^-9. Data were collected from the second leaves on the percentage of withering and the levels of endogenous silicon, malondialdehyde (MDA), hydrogen peroxide (H202), superoxide radical (O2^.-), superoxide dismutase (SOD, EC 1.15.1.1), glutathione peroxidase (GSH-Px, EC 1.11.1.9), ascorbate peroxidase (APX, EC 1.11.1.11), monodehydroascorbate reductase (MDHAR, EC 1.6.5.4), glutathione reductase (GR, EC 1.6.4.2), reduced glutathione (GSH) and ascorbate (AsA). Compared to normal temperatures, chilling resulted in partially withered leaves and increased MDA content. When 0.1 or 1 mmol L^-1 exogenous silicon was combined with chilling, the withering of the cucumber leaves was reduced relative to the original chilling treatment, while the endogenous silicon content was increased, antioxidants such as SOD, GSH-Px, APX, MDHAR, GR, GSH, and AsA were more active, and the levels of H2O2, O2^.-, and MDA were lower. We propose that exogenous silicon leads to greater deposition of endogenous silicon and thereby increases antioxidant activities and reduces lipid peroxidation induced by chilling.

Effects of High Temperature on Antioxidant Enzymes and Lipid Peroxidation in Flag Leaves of Wheat During Grain Filling Period

On the basis of the phytotron, the effects of high temperature （daily average temperature 25, 30, 35 and 40℃, respectively） on antioxidant enzymes and lipid peroxidation in flag leaves of wheat at 50% relative air moisture during grain fastest filling stage [19-21 days after anthesis （DAA）] were studied. The wheat cultivars tested were Yangmai 9 with weak-gluten and Yangmai 12 with medium-gluten. Compared with 25℃, the higher the temperature was, the higher was the MDA content in flag leaves, while lower were the SOD, POD, and CAT activities. SOD and CAT activities in Yangmai 12 appeared to be more sensitive to high temperature than that in Yangmai 9. But POD activity in Yangmai 12 was less sensitive to high temperature. MDA content in Yangmai 12 was higher than that in Yangmai 9. The 1000-grain weight declined with increase in temperature.

Chlamydia trachomatis and sperm lipid peroxidation in infertile men

<abstract>Aim: To relate the presence of anti-Chlamydial trachomatis IgA in semen with sperm lipid membrane peroxidation and changes in seminal parameters. Methods: Semen samples of the male partners of 52 couples assessed for undiagnosed infertility were examined for the presence of IgA antibody against C. trachomatis. The level of sperm membrane lipid peroxidation was estimated by determining the malondialdehyde (MDA) formation. Results: Sperm membrane of infertile males with positive IgA antibodies against C. trachomatis showed a higher level of lipid peroxidation than that of infertile males with negative IgA antibody (P<0.05). There was a positive correlation (P< 0.01) between the level of C. trachomatis antibody and the magnitude of sperm membrane lipid peroxidation. All the other tested semen parameters were found to be similar in the two groups. Conclusion: The activation of immune system by C. trachomatis may promote lipid peroxidation of the sperm membrane. This could be the way by which C. trachomatis affects fertility.

Neuroprotective effects of combined lead and cadmium,as well as N-acetylcysteine,on cerebral cortical neurons following lipid peroxidation injury

BACKGROUND： Studies have reported the antioxidant effects of lead and cadmium in the central nervous system, but very few have addressed the combined toxicity of lead and cadmium. The mechanisms by which these combined heavy metals are toxic, as well as how to protect cells from these agents, remains poorly understood. OBJECTIVE： Primary cultured rat cortical neurons were used to determine the effects of combined lead and cadmium on levels of glutathione peroxidase （GSH-Px）, superoxide dismutase （SOD）, catalase （CAT）, and acetylcholinesterase （ACHE）, as well as malondialdehyde （MDA）, and to evaluate the neuroprotective effects of N-acetylcysteine （NAC）. DESIGN, TIME AND SETTING An in vitro toxicological observation was performed at the Comparative Medicine Center of Yangzhou University from August 2007 to April 2008. MATERIALS： Lead acetate, cadmium acetate, and NAC were purchased from Sigma-Aldrich （St. Louis, USA）. Commercial kits of GSH-Px, SOD, CAT, ACHE, and MDA were purchased from Nanjing Jiancheng Bioengineering Institute, Nanjing, China. METHODS： The cerebral cortical neurons were isolated from newborn Sprague dawley rats at 24 hours after birth and primary cultured for 6 days. Thereafter, the cells were treated with a range of cadmium doses （0, 5.0, and 10.0μmol/L）, lead doses （0, 1.0, and 2.0 μmol/L）, or a combination of the two for 12 hours at 37℃in a 5% CO2 incubator, respectively. In addition, the cells were incubated with different doses of cadmium and/or lead and （0 and 50 μmol/L） NAC for 12 hours to assess the protective effects on cell survival. MAIN OUTCOME MEASURES： The activity of SOD, GSH-Px, CAT, and ACHE, as well as MDA content, in the cell lysates was detected using commercial kits. RESULTS： At 12 hours after treatment, compared to the control group, activity of GSH-Px, SOD, and AChE in the lead, cadmium, or combined treated cells was significantly decreased with increasing doses of cadmium/or lead （P 〈 0.05）, but CAT activity and MDA levels were significantly increased （P 〈 0.05）. The combination of cadmium and lead led to higher levels of toxicity than individual exposure. CONCLUSION： The degree of oxidative damage increased when the two heavy metals were combined. NAC protected neonatal cortical neurons by increasing activity of anti-oxidative enzymes and reducing lipid peroxidation, but the reduction was not statistically significant.