Coccidian infection causes oxidative damage in greenfinches

The main tenet of immunoecology is that individual variation in immune responsiveness is caused by the costs of immune responses to the hosts. Oxidative damage resulting from the excessive production of reactive oxygen species during immune response is hypothesized to form one of such costs. We tested this hypothesis in experimental coccidian infection model in greenfinches Carduelis chloris. Administration of isosporan coccidians to experimental birds did not affect indices of antioxidant protection (TAC and OXY), plasma triglyceride and carotenoid levels or body mass, indicating that pathological consequences of infection were generally mild. Infected birds had on average 8% higher levels of plasma malondialdehyde (MDA, a toxic end-product of lipid peroxidation) than un-infected birds. The birds that had highest MDA levels subsequent to experimental infection experienced the highest decrease in infection intensity. This observation is consistent with the idea that oxidative stress is a causative agent in the control of coccidiosis and supports the concept of oxidative costs of immune responses and parasite resistance. The finding that oxidative damage accompanies even the mild infection with a common parasite highlights the relevance of oxidative stress biology for the immunoecological research.     

Lipid peroxidation and total antioxidant status in patients with breast cancer

Oxidative stress is considered to be involved in the pathophysiology of all cancers. The aim of this study is to examine oxidative stress and antioxidant status in patients with breast cancer by evaluation of the serum levels of total antioxidant capacity (TAC) and lipid peroxidation products as malondialdehyde (MDA) and lipid hydroperoxide and to investigate the relationship between these parameters, oxidative stress and serum lipids and lipoproteins. In our study, serum TAC, MDA, lipid hydroperoxide, HDL-cholesterol, VLDL-cholesterol, LDL-cholesterol, total cholesterol, triacylglycerol (TAG), albumin and uric acid levels of 56-breast cancer patients in different clinical stages and 18 healthy women were determined. Significantly lower-levels of TAC were detected in patients with breast cancer in comparison to controls (2.01 +/- 0.01 mmol/l and 2.07 +/- 0.03 mmol/l, respectively, p < 0.05). Serum MDA levels of the patients were higher compared to the controls (3.64 +/- 0.25 microM and 2.72 +/- 0.22 microM, respectively, p < 0.05). No significant difference between lipid hydroperoxide levels of patients and controls was found (0.33 +/- 0.05 microM and 0.32 +/- 0.01 microM, respectively, p > 0.05). These data show that lower TAC and higher MDA levels i.e. increased oxidative stress may be related to breast cancer.     

N-acetylcysteine amide,a thiol antioxidant,prevents bleomycin-induced toxicity in human alveolar basal epithelial cells (A549)

Abstract

Bleomycin (BLM), a glycopeptide antibiotic from Streptomyces verticillus, is an effective antineoplastic drug. However, its clinical use is restricted due to the wide range of associated toxicities, especially pulmonary toxicity. Oxidative stress has been implicated as an important factor in the development of BLM-induced pulmonary toxicity. Previous studies have indicated disruption of thiol-redox status in lungs (lung epithelial cells) upon BLM treatment. Therefore, this study focused on (1) investigating the oxidative effects of BLM on lung epithelial cells (A549) and (2) elucidating whether a well-known thiol antioxidant, N-acetylcysteine amide (NACA), provides any protection against BLM-induced toxicity. Oxidative stress parameters, such as glutathione (GSH), malondialdehyde (MDA), and antioxidant enzyme activities were altered upon BLM treatment. Loss of mitochondrial membrane potential (ΔΨm), as assessed by fluorescence microscopy, indicated that cytotoxicity is possibly mediated through mitochondrial dysfunction. Pretreatment with NACA reversed the oxidative effects of BLM. NACA decreased the reactive oxygen species (ROS) and MDA levels and restored the intracellular GSH levels. Our data showed that BLM induced A549 cell death by a mechanism involving oxidative stress and mitochondrial dysfunction. NACA had a protective role against BLM-induced toxicity by inhibiting lipid peroxidation, scavenging ROS, and preserving intracellular GSH and ΔΨm. NACA can potentially be developed into a promising adjunctive therapeutic option for patients undergoing chemotherapy with BLM.     

Age-associated analysis of oxidative stress parameters in human plasma and erythrocytes

Oxidative damage accumulation in macromolecules has been considered as a cause of cellular damage and pathology. Rarely, the oxidative stress parameters in healthy humans related to the individual age have been reported. The purpose of this study was to examine the redox status in plasma and erythrocytes of healthy individuals and determine correlations between these parameters and the aging process. The following parameters were used: malondialdehyde (MDA), protein carbonyls (PCO), 4-hydroxy-2,3-trans-nonenal (HNE), reduced glutathione (GSH), glutathione disulfide (GSSG) and uric acid (UA) in blood and plasma samples of 194 healthy women and men of ages ranging from 18 to 84 years. The results indicate that the balance of oxidant and antioxidant systems in plasma shifts in favor of accelerated oxidation during ageing. That is demonstrated by increases of MDA, HNE, GSSG and by the slight decrease of erythrocytic GSH with age. As the content of UA is more determined by metabolic and nutritional influences than by the balance between prooxidants and antioxidants there was no significant age-related change observed. For plasma concentrations of HNE the first time age-dependent reference values for healthy humans are presented.     

Intraspecific variation in the venom of the vermivorous cone snail Conus vexillum

A combination of proteomic and biochemical assays was used to examine variations in the venom of Conus vexillum taken from two locations (Hurgada and Sharm El-Shaikh) in the Red Sea, Egypt. Using MALDI/TOF-MS, a remarkable degree of intra-species variation between venom samples from both locations was identified. To evaluate variability in the cytotoxic effects of Conus venom, mice were injected with the same dose from each location. The oxidative stress biomarkers [malondialdehyde (MDA), protein carbonyl content (PCC)], antioxidants [glutathione (GSH), superoxide dismutase (SOD), catalase (CAT)], total antioxidant capacity (TAC) and nitric oxide (NO), were measured 3, 6, 9 and 12 h post venom injection. The venoms induced a significant increase in the levels of PCC, MDA, NO, GSH and CAT. The venoms significantly inhibited the activity of SOD and reduced the TAC. Toxicological data showed that the venom obtained from Hurgada was more potent than that obtained from Sharm El-Shaikh. It can be concluded that: (1) the venom of the same Conus species from different regions is highly diversified (2) the venoms from different locations reflect clear differences in venom potency and (3) the cytotoxic effects of C. vexillum venom can be attributed to its ability to induce oxidative stress.     

The possible neurobehavioral protective effects of natural antioxidant against phototoxicity attenuation of antimicrobial quinolone group in rats

The fluoroquinolones absorb light in the 320 to 330 nm ultraviolet A (UV‐A) wavelength and produce reactive oxygen species (ROS) such as superoxide anion, hydroxyl radical, and hydrogen peroxide; thus, the photodynamic generation of ROS may be the basis of phototoxicity of quinolones in human beings and animals. This study aimed to evaluate the damaging effects of UV‐A radiation at different periods of exposure on rats' brains administered with ciprofloxacin. Ciprofloxacin administration in UV‐A exposed animals exaggerated the brain‐oxidative stress biomarkers and decreased the locomotor activity. Exposure of rats to UV‐A for 60 minutes induced a significant increase of malondialdehyde (MDA), myeloperoxidase (MPO), and a decrease in the values of superoxide dismutase (SOD), glutathione (GSH) compared to a normal one; these changes were UV‐A exposure time–dependent. However, the administration of vitamin C to the UV‐60‐treated group decreased the values of MDA, MPO, and shifted the values of SOD, GSH toward the normal values. Vitamin C, probably due to its strong antioxidant properties, could improve and partially counteract the toxic effect of UV‐A on oxidative stress parameters and prevent the damage in rat's brain tissues.     

Oxidative effects of inorganic and organic contaminants on haemolymph of mussels

We applied a newly-established method in haemolymph of mussels, Mytilus galloprovincialis, exposed to different concentrations of heavy metals, such as zinc and cadmium and organic pollutants, such as PAHs and lindane, for the detection of total antioxidant capacity (TAC). The susceptibility of exposed mussels was increased in relation to oxidative stress induced by contaminants tested. Oxidative modifications of proteins were estimated by measuring protein carbonyl content (PCC) and malondialdehyde levels (MDA). For PCC measurement, a highly sensitive and accurate ELISA method, which requires only 5 µg of protein, was used. The significant increase of PCC and MDA in haemolymph of exposed mussels reinforces its role as biomarkers of oxidative stress. Significant correlation of TAC assay, PCC and MDA was conducted in order to evaluate the utility of PCC and TAC assay, used in the present study, as tools for determining oxidative effects of pollutants in mussels. The results reinforce the application of PCC method as useful tool for the determination of PCC alterations in haemolymph of mussels exposed to different levels of contaminants. In addition, the TAC method gives encouraging results, concerning its ability to predict antioxidant efficiency in haemolymph of mussels exposed to inorganic and organic contaminants.     

Rat kidney antioxidant response to long-term exposure to flavonol rich red wine

This study evaluated the antioxidant defense system of the rat kidney following chronic exposure to red wine rich in flavonols. Both ethanol and antioxidant non-alcoholic wine components, mainly polyphenols, could contribute to the antioxidant status of kidney. Adult rats were given separately, water, ethanol (12.5%), red wine or alcohol-free red wine. After ten weeks of treatment, blood samples were obtained to determine plasma antioxidant capacity (FRAP, ferric reducing ability of plasma), uric acid and ethanol levels. Kidney tissues (cortex and papilla) were separated to perform measurements of reduced glutathione (GSH), glutathione disulfide (GSSG), lipid peroxidation (malondialdehyde, MDA) and the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The activity of (Na + K)-ATPase, a membrane-bound enzyme, was also assessed. Red wine in plasma, elevated the FRAP without changing the concentration of uric acid; in kidney, it diminished the MDA production and elevated the GSH/GSSG ratio and the activity of CAT and GSH-Px. The activity of SOD did not change. Despite the finding that renal (Na + K)-ATPase activity was upregulated by ethanol, it was not altered by either red wine or alcohol-free red wine. The effects on the antioxidant enzymes could be attributed to ethanol, but the increase in the FRAP and GSH/GSSG ratio is attributed to the non-alcoholic components of red wine. These data suggest that there is an enhancement of the antioxidant defense potential in kidney and plasma, after chronic red wine consumption. Both ethanol and the non-alcoholic antioxidant constituents of red wine could be responsible for these effects.     

Reproduction Is Associated with a Tissue-Dependent Reduction of Oxidative Stress in Eusocial Female Damaraland Mole-Rats (Fukomys damarensis)

Oxidative stress has been implicated as both a physiological cost of reproduction and a driving force on an animal''s lifespan. Since increased reproductive effort is generally linked with a reduction in survival, it has been proposed that oxidative stress may influence this relationship. Support for this hypothesis is inconsistent, but this may, in part, be due to the type of tissues that have been analyzed. In Damaraland mole-rats the sole reproducing female in the colony is also the longest lived. Therefore, if oxidative stress does impact the trade-off between reproduction and survival in general, this species may possess some form of enhanced defense. We assessed this relationship by comparing markers of oxidative damage (malondialdehyde, MDA; protein carbonyls, PC) and antioxidants (total antioxidant capacity, TAC; superoxide dismutase, SOD) in various tissues including plasma, erythrocytes, heart, liver, kidney and skeletal muscle between wild-caught reproductive and non-reproductive female Damaraland mole-rats. Reproductive females exhibited significantly lower levels of PC across all tissues, and lower levels of MDA in heart, kidney and liver relative to non-reproductive females. Levels of TAC and SOD did not differ significantly according to reproductive state. The reduction in oxidative damage in breeding females may be attributable to the unusual social structure of this species, as similar relationships have been observed between reproductive and non-reproductive eusocial insects.     

Development of tumor lysis syndrome (TLS): A potential risk factor in cancer patients receiving anticancer therapy

Tumor lysis syndrome (TLS) is characterized by hyperuricaemia, hyperphosphatemia, hyperkalaemia, as well as hypocalcaemia due to the breakdown of tumor cells undergoing cancer therapy (chemo/radio). Therefore it is of interest to evaluate oxidative stress using selective biological markers [Malondialdehyde (MDA), Superoxide Dismutase (SOD), Glutathione (GSH) and Catalase (CAT)] in TLS. We report the marked differences (statistically significant with control) observed among a selected set of biomarkers of oxidative stress (MDA = 8.66±1.37; SOD = 0.15±0.11; GSH = 2.25±.77; CAT = 0.76±.57) in TLS patients in addition to other conventional biomarkers. Moreover, correlation was investigated among the parameters of oxidative stress and other circulating biomarkers of TLS. Data suggest the use of SOD, MDA, and GSH as potential diagnostic biomarker for TLS with other biomarkers.     

Protective effect of green tea on lead-induced oxidative damage in rat’s blood and brain tissue homogenates

Recent studies have shown that lead (Pb) could disrupt tissue prooxidant/antioxidant balance which lead to physiological dysfunction. Natural antioxidants are particularly useful in such situation. Current study was designed to investigate efficacy of green tea extract (GTE), on oxidative status in brain tissue and blood caused by chronic oral Pb administration in rats. Four groups of adult male rats (each 15 rats) were utilized: control group; GTE-group (oral 1.5% w/v GTE for 6 weeks); Pb-group (oral 0.4% lead acetate for 6 weeks), and Pb+GTE-group (1.5% GTE and 0.4% lead acetate for 6 weeks). Levels of prooxidant/antioxidant parameters [lipid peroxides (LPO), nitric oxides (NO), total antioxidant capacity (TAC), glutathione (GSH), glutathione-S-transferase (GST), superoxide dismutase (SOD)] in plasma, erythrocytes, and brain tissue homogenate were measured using colorimetric methods. Pb concentrations in whole blood and brain tissue homogenate were measured by atomic absorption. In Pb-group, levels of LPO were higher while NO and GSH were lower in plasma, erythrocytes, and brain tissue than controls. TAC in plasma, SOD in erythrocytes, and GST in brain tissue homogenate were lower in Pb-group versus control. GTE co-administrated with Pb-reduced Pb contents, increased antioxidant status than Pb-group. In erythrocytes, Pb correlated positively with LPO and negatively with NO, GSH, SOD, and Hb. In brain tissue homogenate, Pb correlated positively with LPO and negatively with GSH. This study suggests that lead induce toxicity by interfering balance between prooxidant/antioxidant. Treatment of rats with GTE combined with Pb enhances antioxidant/ detoxification system which reduced oxidative stress. These observations suggest that GTE is a potential complementary agent in treatment of chronic lead intoxication.     

Association of exposure to polycyclic aromatic hydrocarbons with inflammation,oxidative DNA damage and renal-pulmonary dysfunctions in barbecue makers in Southern Nigeria

Background:Multiple organ dysfunctions have been linked to exposure to polycyclic aromatic hydrocarbons (PAH) and oxidative stress (OS), oxidative DNA damage, and inflammatory response to PAH have been implicated. The biomarkers of OS (malondialdehyde (MDA), total plasma peroxide (TPP), total antioxidant capacity (TAC), glutathione (GSH), nitric oxide (NO), oxidative stress index (OSI)); 8-hydroxy-2-deoxyguanosine (8-OHdG)); tumor necrosis factor-alpha (TNF-α)); 1-hydroxy pyrene (1-HOP)), serum and urine creatinine, uric acid (UA), estimated glomerular filtration rate (eGFR) and peak expiratory flow rate (PEFR) were assessed in barbecue makers. Methods:One hundred barbecue makers and 50 controls were enrolled into the study. Serum and urine creatinine, UA, TAC, MDA, GSH, NO and TPP were estimated by colorimetry, 8-OHdG and TNF-α by ELISA, PEFR using peak flow meter, 1-HOP by HPLC, eGFR and OSI by calculation. Results:Barbecue makers had lower TAC, PEFR, and higher TNF-α and OS compared to controls (p<0.05). Higher TNF-α, lipid peroxidation, and lower antioxidants were observed in barbecue makers who had worked for >5years compared to <5years (p <0.05). Increasing number of working hours was associated with higher NO, lipid peroxidation, OS and lower antioxidants in barbecue makers (p <0.05). Positive associations were observed between 1-HOP and TPP (r=0.570, p=0.000), OSI (r=0.299, p=0.035) and negative association between TAC and TNF-α (r=-0.209, p=0.037), MDA (r=-0.265, p=0.008) in barbecue makers. Conclusion:Increased lipid peroxidation, OS, inflammation and depressed antioxidants and lung function observed in barbecue makers suggest increased risk of chronic lung conditions which may be associated with exposure to PAH in barbecue fumes.Key Words: Inflammation, Kidney, Lipid Peroxidation, Lung, Oxidative Stress, Polycyclic Aromatic Hydrocarbon     

妊娠期糖尿病患者氧化应激水平变化及临床意义*

目的:研究GDM孕妇与正常孕妇血清MDA、SOD及GSH水平变化,探索它们与GDM之间的相互关系,追踪各组妊娠结局研究其临床意义。方法:选取175例孕妇为研究对象,分为GDM组(93例)和对照组(82例)。采用微量法测定血清丙二醛(MDA)、谷胱甘肽(GSH)及超氧化物歧化酶(SOD)水平,并对妊娠结局进行相关性分析。结果:(1) GDM组年龄、孕前体重、BMI值均高于对照组,GSH和SOD水平均低于对照组,MDA水平高于对照组,差异有统计学意义(P0.05);(2) GDM组MDA水平与孕前体重呈负相关(r=-0.3547,P0.05),SOD水平与新生儿出生体重呈正相关(r=0.3292,P0.05),SOD值与早产之间有密切联系(足月产12.68±0.85 vs.早产8.08±1.18, P 0.05),GSH、SOD水平与孕前体重之间,MDA、GSH水平与新生儿出生体重之间,MDA、GSH水平与早产之间均无明显相关性(P0.05),MDA、GSH和SOD水平与剖宫产及胎膜早破均无明显相关性(P0.05)。结论:GDM存在明显的氧化应激反应,GSH、MDA与SOD可以作为评估GDM氧化应激的有效标志物,其与不良妊娠结局有关。     

Biochemical markers of oxidative stress in Perna viridis exposed to mercury and temperature

Oxidative damage and antioxidant properties have been studied in Perna viridis subjected to short-term exposure to Hg along with temperature (72h) and long-term temperature exposures (14 days) as pollution biomarkers. The elevated thiobarbituric acid reactive substances (TBA-RS) levels observed in gills and digestive gland under exposure to Hg, individually and combined with temperature, as also long-term temperature stress have been assigned to the oxidative damage resulting in lipid peroxidation (LPX). Increased activities of antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), glutathione reductase (GR) and glutathione-S-transferase (GST) both in gills and digestive glands under long-term exposures to temperatures are more prominent to heat rather than cold stress suggesting activation of physiological mechanism to scavenge the ROS produced during heat stress. Also decreased values of reduced glutathione (GSH) on long exposures to temperature stress indicate utilisation of this antioxidant, either to scavenge oxiradicals or act in combination with other enzymes, was more than its production capacity under heat stress. The results suggest that temperature variation does alter the active oxygen metabolism by modulating antioxidant enzyme activities, which can be used as biomarker to detect sublethal effects of pollution.     

Fulminant Hepatic Failure in Rats Induces Oxidative Stress Differentially in Cerebral Cortex,Cerebellum and Pons Medulla

Hepatic Encephalopathy (HE) is one of the most common complications of acute liver diseases and is known to have profound influence on the brain. Most of the studies, available from the literature are pertaining to whole brain homogenates or mitochondria. Since brain is highly heterogeneous with functions localized in specific areas, the present study was aimed to assess the oxidative stress in different regions of brain-cerebral cortex, cerebellum and pons medulla during acute HE. Acute liver failure was induced in 3-month old adult male Wistar rats by intraperitoneal injection of thioacetamide (300 mg/kg body weight for two days), a well known hepatotoxin. Oxidative stress conditions were assessed by free radical production, lipid peroxidation, nitric oxide levels, GSH/GSSG ratio and antioxidant enzyme machinery in three distinct structures of rat brain-cerebral cortex, cerebellum and pons medulla. Results of the present study indicate a significant increase in malondialdehyde (MDA) levels, reactive oxygen species (ROS), total nitric oxide levels [(NO) estimated by measuring (nitrites + nitrates)] and a decrease in GSH/GSSG ratio in all the regions of brain. There was also a marked decrease in the activity of the antioxidant enzymes-glutathione peroxidase, glutathione reductase and catalase while the super oxide dismutase activity (SOD) increased. However, the present study also revealed that pons medulla and cerebral cortex were more susceptible to oxidative stress than cerebellum. The increased vulnerability to oxidative stress in pons medulla could be due to the increased NO levels and increased activity of SOD and decreased glutathione peroxidase and glutathione reductase activities. In summary, the present study revealed that oxidative stress prevails in different cerebral regions analyzed during thioacetamide-induced acute liver failure with more pronounced effects on pons medulla and cerebral cortex. Murthy Ch.R.K—Deceased while in service.     

Inhibition of NADPH oxidase by apocynin promotes myocardial antioxidant response and prevents isoproterenol-induced myocardial oxidative stress in rats

Preventive and/or therapeutic interventions for ischemic heart disease have gained considerable attention worldwide. We investigated the mechanism(s) underlying cardioprotection of apocynin (APO) and whether it attenuates isoproterenol (ISO)-induced myocardial damage in vivo. Thirty-two male Wistar Albino rats were randomised into four groups (n?=?8 for each group): Group I (Control); Group II (ISO), ISO was given intraperitoneally (ip) (150?mg/kg/d) daily for 2 consecutive days; Group III (APO?+?ISO), APO was applied ip 20?mg/kg 30?min before the first ISO administration and continued for the next 2 d after the second ISO administration; Group IV (ISO?+?APO), after the ISO treatment on days 1 and 2, 20?mg/kg APO was given ip on days 3 and 4. Cardioprotective effects of APO were evaluated by biochemical values, histopathological observations and the antiapoptotic relative proteins. Mean blood pressure, heart rate, and electrocardiography (ECG) were also monitored. Malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), total oxidant status (TOS), total antioxidant capacity (TAC), oxidative stress index (OSI), caspase-3 and connexin 43 levels were determined. Major ECG changes were observed in the ISO-treated rats. MDA, TOS, OSI and creatine kinase levels decreased and SOD, CAT, GSH and TAC levels increased, indicating that APO reduced cardiac injury and oxidative stress compared with controls. APO also decreased the number of cardiomyocytes with pyknotic nuclei, inflammatory cell infiltration, intracytoplasmic vacuolisation and myofibrils. APO provides preventive and therapeutic effects on ISO-induced myocardial injury in rats by inhibiting reactive oxygen species production, blocking inflammation and enhancing antioxidant status.     

Alterations in Antioxidant Enzymes During Aging in Humans

The oxidative stress theory of aging offers the best mechanistic elucidation of the aging phenomenon and other age-related diseases. The susceptibility of an individual depends on the antioxidant status of the body. In humans, the antioxidant system includes a number of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), nonenzymatic antioxidants such as glutathione (GSH), protein –SH, ascorbic acid, and uric acid, and dietary antioxidants. Antioxidant enzymes form the first line of defense against reactive oxygen species. In an earlier report, we showed that the plasma antioxidant potential in humans decreases as a function of age and that there are compensatory mechanisms operating in the body which are induced to maintain the antioxidant capacity during aging. In the present study, we report the relationship between human aging and antioxidant enzymes SOD and CAT; we also correlate the activity of these enzymes with the antioxidant capacity of the plasma. Our results show a significantly higher plasma SOD and CAT activity in older individuals than in younger individuals. The induction in activity of SOD and CAT during human aging may be a compensatory response of the individual to an increased oxidative stress.     

Effect of trace elements on the seminal oxidative status and correlation to sperm motility in infertile Saudi males

The impact of trace elements, especially zinc, selenium, copper, and magnesium, on male fertility has gained great interest and significance. Increased oxidative stress and altered trace element levels are probable etiological factors underlying male reproductive dysfunction and infertility. The present study focused on the evaluation of seminal oxidative markers, such as reactive oxygen species (ROS), malondialdehyde (MDA), and total antioxidant capacity (TAC), and trace element levels in the normozoospermic fertile control group (n = 40) and asthenozoospermic infertile group (n = 30). Semen from infertile men exhibited significantly higher ROS and MDA levels accompanied with significant decline in TAC and trace element (zinc and magnesium) levels. Furthermore, a significant correlation was observed between trace elements and oxidative markers with sperm motility. The current study revealed increased lipid peroxidation and oxidant-reductant imbalance that leads to deterioration of semen quality and male infertility. Thus, oxidative stress and trace elements can be considered important biomarkers of male infertility. Measurement of seminal oxidative stress with conventional seminological parameters must be integrated in fertility assessment from early stages to ensure healthy semen characteristics and fertility in men.