Ectopic expression of Olig1 promotes oligodendrocyte formation and reduces neuronal survival in developing mouse cortex.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
L Cai
Publications and source records attributed to L Cai.
Steroidal saponins from Tribulus terrestris.
Three new steroidal saponins were isolated from the fruits of Tribulus terrestris, and their structures were elucidated as (25R,S)-5 alpha-spirostane-12-one-3 beta-ol-3-O-beta-xylopyranosyl(1-->2)- [beta-xylopyranosyl(1-->3)]-beta-glucopyranosyl(1-->4)-[alpha-rhamno- pyranosyl(1-->2)]-beta-galactopyranoside; 26-O-beta-glucopyranosyl-(25S)-5 alpha-furostane-12-one-3 beta,22 alpha,26-triol-3-O-beta-glucopyranosyl(1-->2)-beta-galactopyranoside; 26-O-beta-glucopyranosyl-(25S)-5 alpha-furostane-12-one-3 beta,22 alpha,26-triol-3-O-beta-glucopyranosyl(1-->4)-[alpha- rhamnopyranosyl(1-->2)]-beta-galactopyranoside, respectively, by spectroscopic analysis and color reaction.
Carbohydrate Sequence↗
Protective efficacy of rotavirus 2/6-virus-like particles combined with CT-E29H, a detoxified cholera toxin adjuvant.
Identifying a safe and efficacious mucosal adjuvant is crucial for the development of subunit vaccines against rotavirus and other mucosal pathogens. Moreover, recognition of determinants of protective immunity to rotavirus infection is essential to the design of the means to prevent or control this viral gastrointestinal disease. We have studied the kinetics of systemic and mucosal antibody responses elicited upon mucosal immunization of mice with rotavirus recombinant virus-like particles (rVLPs) alone or combined with a detoxified version of cholera toxin, CT-E29H. CT-E29H has been shown to maintain the adjuvant effect of parental cholera holotoxin. Both inbred BALB/c and outbred CD-1 mice were immunized with rotavirus VP2/6-rVLPs (2/6-VLPs) combined with CT-E29H, orally or intranasally (i.n.), and the comparative efficacy of different formulations was then determined. Rotavirus-specific serum and fecal IgA, IgM, and IgG antibodies were determined by enzyme-linked immunoadsorbent assay (ELISA) weekly (or every other week) following vaccination. Animals then were challenged with a murine rotavirus strain, EDIM. The degree to which vaccinated animals were protected from the wild-type rotavirus challenge was reflected in the levels of viral antigen shed in stools (percent reduction in antigen shedding, PRAS). BALB/c mice immunized by either route produced rotavirus-specific serum IgA, IgM and IgG, as well as fecal IgA and IgG, but not IgM; however, the intranasal immunization induced stronger systemic IgG and IgM responses than did oral immunization. Similar levels of prechallenge rotavirus-specific fecal and serum IgA were detected in both the orally and the i.n. immunized groups. Two immunizations with 2-6VLPs and CT-E29H were sufficient to protect BALB/c mice, regardless of the route of administration. PRAS was 99.6, 98.8, and 98.8% for oral, i.n. and the oral + i.n. groups, respectively; in contrast vaccination with 2/6-VLPs alone was not protective (PRAS = 39%), indicating the critical role of CT-E29H in inducing protective levels of immune responses. Two of four outbred CD-1 mice that were immunized orally with 2/6-VLPs-CT-E29H showed no humoral responses (PRAS, 65%), but four of four i.n. immunized CD-1 mice displayed humoral responses (PRAS, 97.9%). Serum anti-VP6 and VP2 antibodies were detected in all immunoresponsive mice. The combined results in two strains of mice indicate that CTE29H is an effective mucosal adjuvant capable of inducing protective immune responses and suggest that intranasal administration is the preferred route of immunization.
Adjuvants, Immunologic↗
Medical care expenditures for hypertension, its complications, and its comorbidities.
OBJECTIVES: Medical expenditures attributed to hypertension were estimated, including expenditures for cardiovascular complications, other conditions for which hypertensives are at higher risk, and comorbidities (secondary diagnoses) that raise the cost of medical care. This article presents total, per capita, and per condition US expenditures in 1998 according to sex, age, and type of health service. METHODS: A variety of national data sources were used to disaggregate national health expenditures in 1998 by diagnosis. Expenditures for cardiovascular complications and other conditions for which hypertensives had higher rates of utilization were determined by analysis of attributable risks. Additional expenditures generated by extra hospital inpatient days and higher charges for nursing home and home health care for comorbidities were estimated by regression analyses. RESULTS: In 1998, $108.8 billion in health care spending was attributed to hypertension, 12.6% of total national spending that could be allocated to diagnoses, including $22.8 billion for hypertension, $29.7 billion for cardiovascular complications, and $56.4 billion for other diagnoses. Per capita expenditures increased with age from $249 for those younger than 65 years to $3,007 for those 85 years and older. The average amount spent per hypertensive condition was $3,787. Expenditures were generally higher for females. CONCLUSIONS: The economic burden of hypertension is large, but health services directly related to hypertension account for only a fraction of attributed expenditures. Comprehensive accounting of expenditures more accurately assesses the cost of hypertension and potential savings from prevention and treatment. Alteration of lifestyles and medical intervention provide opportunities to reduce national health expenditures.
Adult↗
Angiotensin II activates the GFAT promoter in mesangial cells.
Expression of glutamine:fructose-6-phosphate amidotransferase (GFAT), the rate-limiting enzyme for glucose entry into the hexosamine pathway, is transcriptionally regulated. Immunohistochemical studies of human kidney biopsies demonstrate increased GFAT expression in diabetic glomeruli, but the mechanism responsible for this overexpression is unknown. Given the role of ANG II in diabetic kidney disease, we chose to study the effect of ANG II on GFAT promoter activity in mesangial cells (MC). Exposure of MC to ANG II (10(-7) M) increased GFAT promoter activity (2.5-fold), mRNA (3-fold), and protein (1.6-fold). ANG II-mediated GFAT promoter activation was inhibited by the ANG II type I receptor antagonist candesartan (10(-8) M) but was unaffected by the ANG II type II receptor antagonist PD-123319 (10(-8) M). The intracellular calcium chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (10(-6) M), protein kinase C (PKC) inhibitors bisindoylmaleimide-4 (10(-6) M) and calphostin C (10(-7) M), protein tyrosine kinase (PTK) inhibitor genistein (10(-4) M), Src family kinase inhibitor PP2 (2.5 x 10(-7) M), p42/44 mitogen-activated protein kinase (MAPK) inhibitor PD-98059 (10(-5) M), and the epidermal growth factor (EGF) inhibitor AG-1478 all attenuated GFAT promoter activation by ANG II. We conclude that the GFAT promoter is activated by ANG II via the AT1 receptor. Promoter activation is calcium dependent and PKC dependent but also involves PTK signaling pathways including Src, the EGF receptor, and p42/44 MAPK.
Angiotensin II↗
Iterative algorithm with a constraint condition for numerical reconstruction of a three-dimensional object from its hologram.
A novel method to obtain the three-dimensional mathematical model of a transparent object from its hologram is presented. The proposed method can numerically extract the object information from the fringe pattern of the hologram. Then an iterative algorithm is used to imitate an imaging system by focusing on different layers of the object; and by operating in both the spatial domain and the frequency domain, the algorithm produces a series of two-dimensional layer images. The object is finally reconstructed layer by layer. A constraint condition should be satisfied, and the noise distribution can be rearranged in different reconstruction cycles so as to get better reconstruction quality. Numerical simulations have proved the effectiveness of the proposed method.
Journal Article↗
Oxidative stress and diabetic cardiomyopathy: a brief review.
Diabetes is a serious public health problem. Improvements in the treatment of noncardiac complications from diabetes have resulted in heart disease becoming a leading cause of death in diabetic patients. Several cardiovascular pathological consequences of diabetes such as hypertension affect the heart to varying degrees. However, hyperglycemia, as an independent risk factor, directly causes cardiac damage and leads to diabetic cardiomyopathy. Diabetic cardiomyopathy can occur independent of vascular disease, although the mechanisms are largely unknown. Previous studies have paid little attention to the direct effects of hyperglycemia on cardiac myocytes, and most studies, especially in vitro, have mainly focused on the molecular mechanisms underlying pathogenic alterations in vascular smooth-muscle cells and endothelial cells. Thus, a comprehensive understanding of the mechanisms of diabetic cardiomyopathy is urgently needed to develop approaches for the prevention and treatment of diabetic cardiac complications. This review provides a survey of current understanding of diabetic cardiomyopathy. Current consensus is that hyperglycemia results in the production of reactive oxygen and nitrogen species, which leads to oxidative myocardial injury. Alterations in myocardial structure and function occur in the late stage of diabetes. These chronic alterations are believed to result from acute cardiac responses to suddenly increased glucose levels at the early stage of diabetes. Oxidative stress, induced by reactive oxygen and nitrogen species derived from hyperglycemia, causes abnormal gene expression, altered signal transduction, and the activation of pathways leading to programmed myocardial cell deaths. The resulting myocardial cell loss thus plays a critical role in the development of diabetic cardiomyopathy. Advances in the application of various strategies for targeting the prevention of hyperglycemia-induced oxidative myocardial injury may be fruitful.
Cardiomyopathies↗
Glutathione S-transferases M1, T1 genotypes and the risk of gastric cancer: a case-control study.
AIM: Glutathione S-transferases (GSTs) are involved in the detoxification of many potential carcinogens and appear to play a critical role in the protection from the effects of carcinogens. The contribution of glutathione S-transferases M1 and T1 genotypes to susceptibility to the risk of gastric cancer and their interaction with cigarette smoking are still unclear. The aim of this study was to determine whether there was any relationship between genetic polymorphisms of GSTT1 and GSTT1 and gastric cancer. METHODS: A population based case-control study was carried out in a high-risk area, Changle County, Fujian Province, China. The epidemiological data were collected by a standard questionnaire and blood samples were obtained from 95 incidence gastric cancer cases and 94 healthy controls. A polymerase chain reaction method was used to detect the presence or absence of the GSTT1 and GSTT1 genes in genomic DNA. Logistic regression model was employed in the data analysis. RESULTS: An increase in risk for gastric cancer was found among carriers of GSTT1 null genotype. The adjusted odds ratio (OR) was 2.63 95% Confidence Interval (95% CI) 1.17-5.88, after controlling for age, gender, cigarette smoking, alcohol drinking, and fish sauce intake. The frequency of GSTT1 null genotype in cancer cases (43.16%) was not significantly different from that in controls (50.00%). However, the risk for gastric cancer in those with GSTT1 null and GSTT1 non-null genotype was significantly higher than in those with both GSTT1 and GSTT1 non-null genotype (OR = 2.77, 95% CI 1.15-6.77). Compared with those subjects who never smoked and had normal GSTT1 genotype, ORs were 1.60 (95% CI:0.62-4.19) for never smokers with GSTT1 null type, 2.33 (95% CI 0.88-6.28) for smokers with normal GSTT1, and 8.06 (95% CI 2.83-23.67) for smokers with GSTT1 null type. CONCLUSIONS: GSTT1 gene polymorphisms may be associated with genetic susceptibility of stomach cancer and may modulate tobacco-related carcinogenesis of gastric cancer.
Adult↗
Cytochrome P450 2E1 genetic polymorphism and gastric cancer in Changle, Fujian Province.
AIM: Genetic polymorphism in enzymes of carcinogen metabolism has been found to have the influence on the susceptibility to cancer. Cytochrome P450 2E1 (CYP2E1) is considered to play an important role in the metabolic activation of procarcinogens such as N-nitrosoamines and low molecular weight organic compounds. The purpose of this study is to determine whether CYP450 2E1 polymorphisms are associated with risks of gastric cancer. METHODS: We conducted a population based case-control study in Changle county, Fujian Province, a high-risk region of gastric cancer in China. Ninety-one incident gastric cancer patients and ninety-four healthy controls were included in our study. Datas including demographic characteristics, diet intake, and alcohol and tobacco consumption of individuals in our study were completed by a standardized questionnaire.PCR-RFLP revealed three genotypes:heterozygote (C1/C2) and two homozygotes (C1/C1 and C2/C2) in CYP2E1. RESULTS: The frequency of variant genotypes (C1/C2 and C2/C2) in gastric cancer cases and controls was 36.3% and 24.5%, respectively. The rare homozygous C2/C2 genotype was found in 6 individuals in gastric cancer group(6.6%), whereas there was only one in the control group (1.1%). However, there was no statistically significant difference between the two groups (two-tailed Fisher's exact test P=0.066). Individuals in gastric cancer group were more likely to carry genotype C1/C2 (odds ratio, OR=1.50) and C2/C2 (OR=7.34) than individuals in control group (chi(2) =4.597, for trend P=0.032). The frequencies of genotypes with the C2 allele (C1/C2 and C2/C2 genotypes) were compared with those of genotypes without C2 allele (C1/C1 genotype) among individuals in gastric cancer group and control group according to the pattern of gastric cancer risk factors. The results show that individuals who exposed to these gastric cancer risk factors and carry the C2 allele seemed to have a higher risk of developing gastric cancer. CONCLUSION: Polymorphism of CYP2E1 gene may have some effect in the development of gastric cancer in Changle county, Fujian Province.
Aged↗
Differential effects of doxorubicin on atrial natriuretic peptide expression in vivo and in vitro.
Doxorubicin (Dox) is a potent anti-cancer agent with cardiotoxic side-effects but the mechanism of its cardiotoxicity and its effect on expression of the vasoactive atrial natriuretic peptide (ANP), an important marker for cardiac hypertrophy, are little understood. The present study examined Dox-induced changes in vivo in hearts of 6 mongrel dogs and 5 Sprague-Dawley rats and in vitro in cardiac cultures of neonatal rats. Quantitative RT-PCR analysis using gamma 32-p labeled primers for beta-actin, phospholamban (PLB) and ANP showed a selective 5-fold increase of ANP mRNA in Dox-treated dog hearts in comparison to controls. Similarly, northern analysis of GAPD, beta-actin, cardiac alpha-actin and ANP gave a selective 4.5-fold increase in ANP transcripts in Dox-treated rat hearts. On the other hand, there was a selective decrease (approximately 39%) of ANP transcripts in Dox-treated cardiac cultures relative to controls. Immunohistochemistry localized the ANP changes both in tissue sections and in cultures to the cardiomyocytes. The data clearly showed that Dox selectively increases ANP expression in dog and rat hearts in absence of cardiocyte hypertrophy but selectively decreases it in cardiac cultures. This differential effect of Dox on cardiocytes in vivo and in vitro should be a useful parameter for studies of transcriptional control of ANP expression.
Animals↗
Apolipoprotein A-I conformation markedly influences HDL interaction with scavenger receptor BI.
Apolipoprotein A-I (apoA-I) is an important ligand for the high density lipoprotein (HDL) scavenger receptor class B type I (SR-BI). SR-BI binds both free and lipoprotein-associated apoA-I, but the effects of particle size, composition, and apolipoprotein conformation on HDL binding to SR-BI are not understood. We have studied the effect of apoA-I conformation on particle binding using native HDL and reconstituted HDL particles of defined composition and size. SR-BI expressed in transfected Chinese hamster ovary cells was shown to bind human HDL(2) with greater affinity than HDL(3), suggesting that HDL size, composition, and possibly apolipoprotein conformation influence HDL binding to SR-BI. To discriminate between these factors, SR-BI binding was studied further using reconstituted l-alpha-palmitoyloleoyl-phosphatidylcholine-containing HDL particles having identical components and equal amounts of apoA-I, but differing in size (7.8 vs. 9.6 nm in diameter) and apoA-I conformation. The affinity of binding to SR-BI was significantly greater (50-fold) for the larger (9.6-nm) particle than for the 7.8-nm particle. We conclude that differences in apoA-I conformation in different-sized particles markedly influence apoA-I recognition by SR-BI. Preferential binding of larger HDL particles to SR-BI would promote productive selective cholesteryl ester uptake from larger cholesteryl ester-rich HDL over lipid-poor HDL.
Apolipoprotein A-I↗
[Molecular characterization of glucose-6-phosphate dehydrogenase deficiency in the Han and Li nationalities in Hainan, China and identification of a new mutation in human G6PD gene].
OBJECTIVE: To elucidate the molecular basis of G6PD deficiency in the Han and Li nationalities in Hainan, China. METHODS: Polymerase chain reaction and restriction enzyme digestion were used to screen the mutations 1388G-->A, 1360C-->T, 1024C-->T, 592C-->T, 517T-->C, 493A-->G, 487G-->A, 392G-->T and 95A-->G. Single strand conformation polymorphism analysis was used to screen the other mutations followed by DNA sequencing to characterize the mutations of the samples with abnormal SSCP bands. RESULTS: Of the fifty-nine Han cases with G6PD deficiency, fourteen with 1388G-->A (23.7%), three with 871G-->A(5.1%), one with 835A-->T(1.7%), one with 517T-->C (1.7%), three with 392G-->T(5.1%), and four with 95A-->G(6.8%) were found. Of the thirty-two Li cases with G6PD deficiency, six with 1388G-->A(18.8%), three with 871G-->A(9.4%), and two with 95A-->G(6.3%) were found. A new mutation 835A-->G which causes the substitution of Ala for Thr at 279 in a Han case was identified and named as G6PD Haikou. The enzyme activity of the variant is about 10% of the normal and lower than the activity of the variant 835A-->T with about 40% of the normal. Analysis of the 3D model of human G6PD has revealed that the hydroxyl group of Thr at 279 is a group in maintaining the interaction of the G6PD subunits. CONCLUSION: The most common mutations of G6PD deficiency in Han and Li nationalities in Hainan are similar. Compared with the mutation spectrum of G6PD gene in the populations in other regions of China, the results indicate that some G6PD gene mutations are widespread in the populations of different regions in the southern part of China. The hydroxyl group of the Thr at 279 of human G6PD may be a necessary group for maintaining the interaction of the G6PD subunits and the enzyme activity.
Child↗
CD36 does not play a direct role in HDL or LDL metabolism.
CD36 and scavenger receptor class B, type I (SR-BI) are both class B scavenger receptors that recognize a broad variety of ligands, including oxidized low density lipoprotein (oxLDL), HDL, anionic phospholipids, and apoptotic cells. In this study we investigated the role of mouse CD36 (mCD36) as a physiological lipoprotein receptor. We compared the association of various lipoprotein particles with mCD36 and mSR-BI expressed in COS cells by adenovirus-mediated gene transfer. mCD36 bound human oxLDL and mouse HDL with high affinity. Human LDL bound poorly to mCD36, indicating that mCD36 is unlikely to play a significant role in LDL metabolism. The ability of mCD36 to mediate the selective uptake of cholesteryl esters (CE) from receptor-bound HDL was assessed. In comparison with mSR-BI, mCD36 inefficiently mediated the selective uptake of CE. Hepatic overexpression of mCD36 in C57BL/6 mice by adenovirus-mediated gene transfer did not result in significant alterations in plasma LDL and HDL levels. We conclude that mCD36, while able to bind HDL with high affinity, does not contribute significantly to HDL or LDL metabolism.
Adenoviridae↗
[Studies on the chemical components from Sargassum fusiform].
Three compounds have been isolated from Sargassum fusiform collected from nanao island. Based on the spectral data and elemental analysis, they were identified as 2,4-dihydroxy-2,6-trimethyl-delta 1,alpha-cyclohexaneacetic-r-lactone, saringosterol and cedrol.
Cyclohexanes↗
[Study on the relationship between apoptosis and reactive oxygen species of cancer cell lines induced by anticarcinogens].
OBJECTIVE: To investigate the relationship between apoptosis (AP) and fluorescent intensity of reactive oxygen species (ROS) in cancer cell lines induced by anticancer agents, and the mechanisms of drug sensitivity and resistance. METHOD: K562 cells were treated respectively with each of the Vp16, ADR and DDP, the fluorescent intensity of ROS and AP percentage of K562 cells at different concentration of the drugs treated were assayed by flow cytometry (FCM). RESULT: (1) After treatment with these drugs for 24 hours, the fluorescent intensity of ROS and AP percentage of K562 cells increased obviously as compared with that of control groups. (2) The optimum concentrations of the drugs for ROS production and AP of K562 cells were determined. CONCLUSION: Anticancer agents induced AP of K562 cells, which might be through stimulating ROS production.
Antineoplastic Agents↗
Assessing the resectability of pancreatic ductal adenocarcinoma: comparision of dual-phase helical CT arterial portography with conventional angiography.
OBJECTIVE: To evaluate the respective value of dual-phase helical CT arterial portography (CTAP) and conventional angiography in preoperative predicting resectability of pancreatic ductal adenocarcinoma. SUBJECTS AND METHODS: Tumor resectability was prospectively evaluated in 54 patients with pathologically proven pancreatic ductal adenocarcinoma who later underwent surgery. Both dual-phase helical CT scanning and selective angiography were obtained in each patient preoperatively. For optimal enhancement of pancreas and major peripancreatic vessels, two catheters connected to an automatic injector via a Y-shaped tube were placed selective angiography, one in celiac trunk, the other in superior mesenteric artery. Then the patient underwent dual-phase helical CTAP of pancreas and liver. The criteria of irresectability for CTAP include: tumor diameter > or = 5 cm, extrapancreatic invasion, distant metastases and vascular involvement (occlusion, stenosis or semicircular encasement of superior mesenteric artery, hepatic artery, splenic artery, celiac axis; portal vein, superior mesenteric vein or splenic vein). The results of both modalities were correlated with findings from surgery or pathology. RESULTS: Thirty-eight of 54 patients had nonresectable disease. In prediction the irresectability, sensitivity, specificity, positive predictive value, negative predictive value and overall accuracy were 94.7%, 100%, 100%, 88.9%, 96.3% respectively for helical CTAP and 63.2%, 93.89%, 96.0%, 51.7%, 72. 2% respectively for selective angiography. In assessing vascular involvements, dual-phase helical CTAP was also superior to selective angiography. CONCLUSION: Dual-phase helical CTAP is superior to angiography in assessing resectability of pancreatic ductal adenocarcinoma. The combination of the two modalities may further improve overall creatic
Adenocarcinoma↗
NO inhibits stretch-induced MAPK activity by cytoskeletal disruption.
Mesangial cells (MC) grown on extracellular matrix protein-coated plates and exposed to cyclic strain/relaxation proliferate and produce extracellular matrix protein, providing an in vitro model of signaling in stretched MC. Intracellular transduction of mechanical strain involves mitogen-activated protein kinases, and we have shown that p42/44 mitogen-activated protein kinase (extracellular signal-regulated kinase (ERK)) is activated by cyclic strain in MC. In vivo studies show that increased production of nitric oxide (NO) in the remnant kidney limits glomerular injury without reducing glomerular capillary pressure, and we have observed that NO attenuates stretch-induced ERK activity in MC via generation of cyclic guanosine monophosphate (cGMP). Accordingly, we sought to determine whether NO affects strain-induced ERK activity after strain and how this is mediated. Strain-induced ERK activity was dependent on time and magnitude of stretch and was maximal after 10 min at -27 kilopascals. Actin cytoskeleton disruption with cytochalasin D abrogated this. The non-metabolizable cGMP analogue 8-bromo cyclic GMP (8-Br-cGMP) dose-dependently attenuated strain-induced ERK activity. Cytoskeletal stabilization with jasplakinolide prevented this inhibitory effect of 8-Br-cGMP. Cyclic strain increased nuclear translocation of phospho-ERK by immunofluorescent microscopy, again attenuated by 8-Br-cGMP. Jasplakinolide prevented the inhibitory effect of 8-Br-cGMP on activated ERK nuclear translocation after strain. Strain increased ERK-dependent AP-1 nuclear protein binding, which was attenuated by cytochalasin D and 8-Br-cGMP. These data indicate that cGMP can inhibit cyclic strain-induced ERK activity, nuclear translocation, and AP-1 nuclear protein binding. Cytoskeletal disruption leads to the same effect, whereas cytoskeleton stabilization reverses the effect of 8-Br-cGMP. Thus, NO inhibits strain-induced ERK activity by cytoskeletal destabilization.
Actins↗
Metallothionein inhibits peroxynitrite-induced DNA and lipoprotein damage.
Previous studies have demonstrated that metallothionein functions as an antioxidant that protects against oxidative DNA, protein, and lipid damage induced by superoxide anion, hydrogen peroxide, hydroxyl radical, and nitric oxide. The present study was undertaken to test the hypothesis that metallothionein also protects from DNA and lipoprotein damage induced by peroxynitrite, an important reactive nitrogen species that causes a diversity of pathological processes. A cell-free system was used. DNA damage was detected by the mobility of plasmid DNA in electrophoresis. Oxidation of low density lipoprotein was measured by a thiobarbituric acid-reactive substance, which was confirmed by lipid hydroperoxide assay. Plasmid DNA damage and low density lipoprotein oxidation were induced by 3-morpholinosydnomine, which produces peroxynitrite through the reaction between nitric oxide and superoxide anion or by synthesized peroxynitrite directly. DNA damage by 3-morpholinosydnomine was prevented by both metallothionein and superoxide dismutase, whereas the damage caused by peroxynitrite was prevented by metallothionein only. The oxidation of low density lipoprotein by 3-morpholinosydnomine and peroxynitrite was also significantly inhibited by metallothionein. This study thus demonstrates that metallothionein may react directly with peroxynitrite to prevent DNA and lipoprotein damage induced by this pathological reactive nitrogen species.
Antioxidants↗