OBJECTIVES: Malondialdehyde (MDA), a lipid peroxidation by-product, has been widely used as an indicator of oxidative stress. Urinary 2-naphthol, a urinary PAH metabolite, is used as a marker of ambient particulate exposure and is associated with lung cancer and chronic obstructive pulmonary disease. However, the stability and intra-individual variation associated with urinary MDA and 2-naphthol have not been thoroughly addressed. The objective of this study was to assess the stability and intraindividual variation associated with urinary MDA and 2-naphthol. METHODS: Urine samples were collected from 10 healthy volunteers (mean age 34, range 27~42 years old). Each sample was divided into three aliquots and stored under three different conditions. The levels of urinary MDA and 2-naphthol were analyzed 1) just after sampling, 2) after storage at room temperature (21degrees C) for 16 hours, and 3) after storage in a -20degrees C freezer for 16 hours. In addition, an epidemiological study was conducted in 44 Chinese subjects over a period of 3 weeks. The urinary MDA and 2-naphthol were measured by HPLC three times. RESULTS: There was no difference in the levels of urinary MDA and 2-naphthol between the triplicate measurements (n=10, p=0.84 and p=0.83, respectively). The intra-class correlation coefficients (ICC) for urinary MDA and 2-naphthol were 0.74 and 0.42, respectively. However, the levels of PM2.5 in the air were well correlated with the levels of both MDA and 2-naphthol in the epidemiological study. CONCLUSIONS: These results suggest that urinary MDA and 2-naphthol remain stable under variable storage conditions, even at room temperature for 16 hours, and indicate that these markers can be used in epidemiological studies involving various sample storage conditions. The intra-CC of urinary 2-naphthol and MDA were acceptable for application to epidemiological studies.
Adult ; Biological Markers ; Female ; Humans ; Male ; Malondialdehyde/*metabolism/*urine ; Middle Aged ; Naphthols/*metabolism/*urine ; Oxidative Stress/physiology ; Reproducibility of Results

OBJECTIVETo investigate whether a simulated He-O2 saturation dive to 65 msw would affect oxidative balance in humans.

METHODSSeven divers participated in a simulated saturation dive to 0.75 MPa (65 msw). 24-h urine samples were collected twice before, twice during, and twice after the dive, then were analyzed for contents of superoxide dismutase (SOD), malondialdehyde (MDA), total amino acid (T-AA) and total anti-oxidant capacity (T-AOC). Meanwhile, total urine volume and body weight were measured.

RESULTSThe content of T-AA was higher. (P < 0.05) than the base value in final decompression, but reverse to normal at one week after decompression. There were no changes in contents of SOD, MDA and T-AOC during and after the dive compared with their basic value. Total urine volume was lower (P < 0.05, vs basic value) at first day in chamber, then returned to normal. Body weight gradually increased after compression till the end of decompression (higher than basic value, P < 0.05).

CONCLUSIONThese data indicate that simulated saturation dive to 65 msw may not induce obvious oxidative damage, but it is necessary to monitor 24-h urine volume and oxidative sress by time in order to prevent from tissue injury.

Adult ; Amino Acids ; urine ; Decompression ; Diving ; physiology ; Helium ; chemistry ; Humans ; Male ; Malondialdehyde ; urine ; Oxidative Stress ; physiology ; Oxygen ; adverse effects ; chemistry

This study was aimed to evaluate renal dysfunction during three weeks after the burn injuries in 12 patients admitted to the Hallym University Hankang Medical Center with flame burn injuries (total body surface area, 20-40%). Parameters assessed included 24-hr urine volume, blood urea nitrogen, serum creatinine, creatinine clearance, total urinary protein, urinary microalbumin, 24-hr urinary N-acetyl--D-glucosaminidase (NAG) activity, and urinary malondialdehyde (MDA). Statistical analysis was performed using repeated measures ANOVA test. The 24-hr urine volume, creatinine clearance, and urinary protein significantly increased on day 3 post-burn and fell thereafter. The urine microalbumin excretion showed two peak levels on day 0 post-burn and day 3. The 24-hr urinary NAG activity significantly increased to its maximal level on day 7 post-burn and gradually fell thereafter. The urinary MDA progressively increased during 3 weeks after the burn injury. Despite recovery of general renal function through an intensive care of burn injury, renal tubular damage and lipid peroxidation of the renal tissue suggested to persist during three weeks after the burn. Therefore, a close monitoring and intensive management of renal dysfunction is necessary to prevent burn-induced acute renal failure as well as to lower mortality in patients with major burns.
Acetylglucosaminidase/*urine ; Adult ; Aged ; Albuminuria/etiology ; Biological Markers ; Burns/*complications ; Female ; Human ; Kidney Diseases/*diagnosis/urine ; Kidney Failure, Acute/diagnosis ; Lipid Peroxidation ; Male ; Malondialdehyde/*urine ; Middle Age

It is not well described the pathophysiology of renal injuries caused by a high salt intake in humans. The authors analyzed the relationship between the 24-hr urine sodium-to-creatinine ratio (24HUna/cr) and renal injury parameters such as urine angiotensinogen (uAGT/cr), monocyte chemoattractant peptide-1 (uMCP1/cr), and malondialdehyde-to-creatinine ratio (uMDA/cr) by using the data derived from 226 hypertensive chronic kidney disease patients. At baseline, the 24HUna/cr group or levels had a positive correlation with uAGT/cr and uMDA/cr adjusted for related factors (P<0.001 for each analysis). When we estimated uAGT/cr in the 24HUna/cr groups by ANCOVA, the uAGT/cr in patients with > or =200 mEq/g cr was higher than in patients with <100 mEq/g cr (708 [95% CI, 448-967] vs. 334 [95% CI, 184-483] pg/mg cr, P=0.014). Similarly, uMDA/cr was estimated as 0.17 (95% CI, 0.14-0.21) pM/mg cr in patients with <100 mEq/g cr and 0.27 (95% CI, 0.20-0.33) pM/mg cr in patients with > or =200 mEq/g cr (P=0.016). During the 16-week follow-up period, an increase in urinary sodium excretion predicted an increase in urinary angiotensinogen excretion. In conclusion, high salt intake increases renal renin-angiotensin-system (RAS) activation, primarily, and directly or indirectly affects the production of reactive oxygen species through renal RAS activation.
Adult ; Aged ; Angiotensinogen/urine ; Chemokine CCL2/urine ; Creatine/urine ; Demography ; Female ; Follow-Up Studies ; Humans ; Hypertension/complications ; Male ; Malondialdehyde/urine ; Middle Aged ; Reactive Oxygen Species/*metabolism ; Renal Insufficiency, Chronic/complications/*pathology ; Renin-Angiotensin System/*physiology ; Sodium, Dietary/*urine ; Urine Specimen Collection

OBJECTIVETo evaluate the effect of dibutyl phthalate (DBP) and di-(2-ethylhexyl) phthalate (DEHP) on urine superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in rats.

METHODSAccording to 2×2 factorial analysis, 60 adult male SD rats were randomized into 10 groups (n=6), including a control group (fed with sesame oil), 3 DBP groups (fed with DBP at the doses of 30, 100 and 300 mg/kg), 3 DEHP groups (with DEHP at 50, 150, and 450 mg/kg), and 3 DBP+DEHP groups (with 30 mg/kg DBP+50 mg/kg DEHP, 100 mg/kg DBP+150 mg/kg DEHP, and 300 mg/kg DBP +450 mg/kg DEHP). The agents were administered in a single dose through gavage in a volume of 2 ml. After the treatments, the 24, 48, 72, and 96 h urine samples were collected to determine the SOD activity and MDA content.

RESULTSDBP and DEHP, either alone or in combination, significantly decreased SOD activity and increased MDA content in the urine collected at 24 h but not at the other time points. Such changes were gradually reversed with time.

CONCLUSIONDBP or DEHP treatment alone can result in significant oxidative damage in the kidney of rats, and the toxic effect of the combined exposure is even more obvious.

Animals ; Dibutyl Phthalate ; toxicity ; Diethylhexyl Phthalate ; toxicity ; Environmental Pollutants ; toxicity ; Kidney ; drug effects ; physiopathology ; Male ; Malondialdehyde ; urine ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; urine

OBJECTIVEThis study aims to investigate the protection of procyanidins and lycopene from the renal damage induced by mercuric chloride.

METHODSRats were treated with either procyanidins or lycopene 2h before HgCl(2) subcutaneously injection, once daily treatment for 2 successive days.

RESULTSIn comparison with HgCl(2) group, markers of renal function such as blood urea nitrogen in serum and urinary protein were decreased to (18.45±11.63) mmol/L and (15.93±9.36) mmol/L, (4.54±0.78) g/(g·Cr) and (4.40±1.12) g/(g·Cr). N-acetyl-beta-D-glucosaminidase, lactate dehydrogenase, alkaline phosphatase in urine were depressed to (125.49±11.68) U/(g·Cr), (103.73±21.79) U/(g·Cr), (101.99±12.28) U/(g·Cr), and (113.19±23.74) U/(g·Cr), (71.14±21.80) U/(g·Cr), (73.64±21.51) U/(g·Cr) in procyanidins and lycopene groups. Indicators of oxidative stress, for example, Glutathion was reduced to (45.58±9.89) μmol/(g·pro) and (45.33±5.90) μmol/(g·pro), and antioxidant enzymes such as superoxide dismutase, glutathione-peroxidase were enhanced to (43.07±10.97) U/(mg·pro) and (39.94±6.04) U/(mg·pro), (83.85±18.48) U/(mg·pro), and (85.62±12.68) U/(mg·pro). Malondialdehyde was lowered to (0.95±0.12) (μmol/g·pro) and (1.03±0.12) μmol/(g·pro) in procyanidins and lycopene groups. ROS generation was decreased by 27.63% and 16.40% and apoptosis was also decreased in procyanidins and lycopene groups respectively. Pathological changes were much better as well.

CONCLUSIONProcyanidins and Lycopene play some protective role against mercury kidney damage.

Acetylglucosaminidase ; urine ; Alkaline Phosphatase ; urine ; Animals ; Antioxidants ; therapeutic use ; Blood Urea Nitrogen ; Carotenoids ; therapeutic use ; Glutathione ; metabolism ; Glutathione Peroxidase ; metabolism ; Kidney ; drug effects ; metabolism ; pathology ; Kidney Diseases ; chemically induced ; metabolism ; pathology ; prevention & control ; L-Lactate Dehydrogenase ; urine ; Lipid Peroxidation ; Malondialdehyde ; metabolism ; Mercuric Chloride ; pharmacokinetics ; toxicity ; urine ; Mercury ; metabolism ; Proanthocyanidins ; therapeutic use ; Rats ; Rats, Wistar ; Reactive Oxygen Species ; metabolism ; Superoxide Dismutase ; metabolism

OBJECTIVEThis report aims to describe the oxidative damage profile in brain of presenilin1 and presenilin2 conditional double knockout mice (dKO) at both early and late age stages, and to discuss the correlation between oxidative stress and the Alzheimer-like phenotypes of dKO mice.

METHODSThe protein level of Abeta(42) in dKO cortex and free 8-OHdG level in urine were measured by ELISA. Thiobarbituric acid method and spectrophotometric DNPH assay were used to determine the lipid peroxidation and protein oxidation in cortex, respectively. SOD and GSH-PX activities were assessed by SOD Assay Kit-WST and GSH-PX assay kit, separately.

RESULTSSignificant decrease of Abeta(42) was verified in dKO cortex at 6 months as compared to control mice. Although lipid peroxidation (assessed by MDA) was increased only in dKO cortex at 3 months and protein oxidation (assessed by carbonyl groups) was basically unchanged in dKO cortex, ELISA analysis revealed that free 8-OHdG, which was an indicator of DNA lesion, was significantly decreased in urine of dKO mice from 3 months to 12 months. Activities of SOD and GSH-PX in dKO and control cortices showed no statistical difference except a significant increase of GSH-PX activity in dKO mice at 9 months.

CONCLUSIONOxidative damage, especially DNA lesion, was correlated with the neurodegenerative symptoms that appeared in dKO mice without the deposition of Abeta(42). Triggers of oxidative damage could be the inflammatory mediators released by activated microglia and astrocytes.

Age Factors ; Alzheimer Disease ; genetics ; metabolism ; physiopathology ; Amyloid beta-Peptides ; urine ; Animals ; Deoxyguanosine ; analogs & derivatives ; urine ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; methods ; Glutathione ; metabolism ; Hydrazines ; metabolism ; Lipid Peroxidation ; genetics ; Malondialdehyde ; metabolism ; Mice ; Mice, Inbred CBA ; Mice, Knockout ; physiology ; Oxidation-Reduction ; Oxidative Stress ; physiology ; Peptide Fragments ; urine ; Presenilin-1 ; deficiency ; Presenilin-2 ; deficiency ; Spectrophotometry, Atomic ; methods ; Superoxide Dismutase ; metabolism

OBJECTIVETo study the effect of terephthalic acid (TPA) on lipid metabolism in Sprague-Dawley (SD) rats.

METHODSFive groups of SD rats that ingested 0%, 0.04%, 0.2%, 1%, and 5% TPA, respectively, were included in a 90-day subchronic feeding study. Effects of TPA on levels of serum protein, total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL), total antioxidative capability (T-AOC), superoxide dismutase (SOD) and malondialdehyde (MDA) were observed. Urine samples were collected and analyzed for concentration of ion.

RESULTSTPA decreased the level of serum T-AOC in a dose dependent manner. The contents of serum and bladder MDA significantly decreased in 1% and 5% TPA ingestion groups. Serum CuZn superoxide dismutase (CuZnSOD) lowered in groups of 0.2%, 1%, and 5% TPA. TPA subchronic feeding had no significant influences on serum TC, LDL or HDL, but increased serum TG, TP and ALB after administration of 0.04% and/or 0.2% TPA. Concentrations of urinary Ca2+, Mg2+, Na+, and K+ were elevated in 1% and 5% TPA groups.

CONCLUSIONAntioxidative potential decreased after TPA exposure. MDA increase in serum and bladder tissues was one of the most important reactions in rats which could protect themselves against TPA impairment. The decrease of serum CuZnSOD was related to the excretion of Zn2+.

Animals ; Antioxidants ; analysis ; Blood Proteins ; analysis ; Cholesterol ; blood ; Female ; Ions ; urine ; Lipid Metabolism ; drug effects ; Lipoproteins ; blood ; Male ; Malondialdehyde ; blood ; Phthalic Acids ; toxicity ; Rats ; Rats, Sprague-Dawley ; Superoxides ; blood ; Triglycerides ; blood ; Weight Gain

Ammonium perchlorate (AP), mainly used as solid propellants, was reported to interfere with homeostasis via competitive inhibition of iodide uptake. However, detailed mechanisms remain to be elucidated. In this study, AP was administered at 0, 130, 260 and 520 mg/kg every day to 24 male SD rats for 13 weeks. The concentrations of iodine in urine, serum thyroid hormones levels, total iodine, relative iodine and total protein, and malondialdehyde (MDA), superoxide dismutase (SOD) and catalase (CAT) activity in thyroid tissues were measured, respectively. Our results showed that high-dose perchlorate induced a significant increase in urinary iodine and serum thyroid stimulating hormone (TSH), with a decrease of total iodine and relative iodine content. Meanwhile, free thyroxine (FT4) was decreased and CAT activity was remarkably increased. Particularly, the CAT activity was increased in a dose-dependent manner. These results suggested that CAT might be enhanced to promote the synthesis of iodine, resulting in elevated urinary iodine level. Furthermore, these findings suggested that iodine in the urine and CAT activity in the thyroid might be used as biomarkers for exposure to AP, associated with thyroid hormone indicators such as TSH, FT4.
Analysis of Variance ; Animals ; Catalase ; metabolism ; Dose-Response Relationship, Drug ; Homeostasis ; drug effects ; Iodine ; metabolism ; urine ; Male ; Malondialdehyde ; metabolism ; Perchlorates ; pharmacology ; Quaternary Ammonium Compounds ; pharmacology ; Radioimmunoassay ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism ; Thyroid Gland ; metabolism ; Thyrotropin ; blood ; Thyroxine ; blood ; Triiodothyronine ; blood

OBJECTIVETo study the effect of fluoride on the oxidative stress of the rats in endemic fluorosis of coal burning and Mn-SOD expression at mRNA and protein levels.

METHODSSD rats were divided into 2 groups (the number of female and male in each group was the same): control group and fluorosis group. All rats of the fluorosis group were fed corn dried by burning coal from endemic fluorosis areas with high fluoride content (fluoride 17 mg/kg in feed) to establish an animal model of fluorosis. In these rats, dental fluorosis was evaluated. The fluoride content in the urine was measured by fluorine ion-elective electrode method. The hepatic tissue and serum level of malonaldehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathion reductase (GR) were measured by biochemical methods. The index signs of liver function were also measured from the serum. Reverse transcription-polymerase chain reaction (RT-PCR) and Western blot were performed to detect the alterations of Mn-SOD expression in the liver at mRNA and protein levels.

RESULTSThe dental fluorosis was observed in the fluorosis group, and the incidence was 11/11. The fluoride contents [(3.50 ± 2.58) mg/L] in the urine of fluorosis rats were increased as compared with the control [(1.42 ± 0.38) mg/L] (P < 0.05). AST [(223.74 ± 71.51) U/L] and total protein [(72.43 ± 5.59) g/L] of the hepatic function index in fluorosis rats showed obviously abnormal as compared with the control [(169.28 ± 53.74) U/L and (82.36 ± 7.31) g/L], respectively (P < 0.05). In the liver the content of MDA [(10.41 ± 0.59) µmol/g protein] increased as compared to the control [(5.80 ± 1.31) µmol/g protein, P < 0.01], and the activities of SOD [(62.60 ± 8.65) U/mg protein] and GR [ (1.17 ± 0.66) U/g protein] markedly decreased in the fluorosis group compared to the control [SOD (117.28 ± 8.64) U/mg protein and GR [(8.80 ± 1.59) U/g protein; P < 0.05, P < 0.01]. The level of Mn-SOD in the liver was markedly decreased in the fluorosis group [(14.83 ± 2.50) U/mg protein] as compared with the control [(34.05 ± 5.22) U/mg protein, P < 0.01]. The levels of mRNA (0.64 ± 0.15) and protein (0.84 ± 0.13) of Mn-SOD were markedly decreased in the fluorosis group as compared with the control [(0.86 ± 0.21) and (1.04 ± 0.14)], respectively (P < 0.05, P < 0.01).

CONCLUSIONSFluorosis can decrease the activities of Mn-SOD, which is associated with decreased levels of mRNA and protein of Mn-SOD. Down-regulation of Mn-SOD expression may play an important role in the aggravation of oxidative stress in endemic fluorosis.

Animals ; Coal ; Down-Regulation ; Female ; Fluorides ; urine ; Fluorosis, Dental ; metabolism ; Glutathione Reductase ; blood ; metabolism ; Liver ; metabolism ; Liver Function Tests ; Male ; Malondialdehyde ; blood ; metabolism ; Oxidative Stress ; RNA, Messenger ; metabolism ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; blood ; genetics ; metabolism