Biomedical subjects

Y Ke

Publications and source records attributed to Y Ke.

At least 19 recordsLinked to original sources

PubMed2006

Depletion of reduced glutathione enhances motor neuron degeneration in vitro and in vivo.

The mechanism of selective and age-dependent motor neuron degeneration in human amyotrophic lateral sclerosis (ALS) has not been defined and the role of glutathione (GSH) in association with motor neuron death remains largely unknown. A motor neuron-like cell culture system and a transgenic mouse model were used to study the effect of cellular GSH alteration on motor neuron cell death. Exposure of NSC34 motor neuron-like cells to ethacrynic acid (EA) or l-buthionine sulfoximine (BSO) dramatically reduced the cellular GSH levels, and was accompanied by increased production of reactive oxygen species (ROS) measured by the dichlorofluorescin (DCF) fluorescent oxidation assay. In addition, GSH depletion enhanced oxidative stress markers, AP-1 transcriptional activation, c-Jun, c-Fos and heme oxygenase-1 (HO-1) expression in NSC34 cells analyzed by a luciferase reporter, Western blotting and quantitative PCR assays respectively. Furthermore, depletion of GSH decreased mitochondrial function, facilitated apoptosis inducing factor (AIF) translocation, cytochrome c release, and caspase 3 activation, and consequently led to motor neuron-like cell apoptosis. In an ALS-like transgenic mouse model overexpressing mutant G93A-Cu, Zn-superoxide dismutase (SOD1) gene, we showed that the reduction of GSH in the spinal cord and motor neuron cells is correlated with AIF translocation, caspase 3 activation, and motor neuron degeneration during ALS-like disease onset and progression. Taken together, the in vitro and in vivo data presented in the current report demonstrated that decreased GSH promotes multiple apoptotic pathways contributing, at least partially, to motor neuron degeneration in ALS.

Amyotrophic Lateral Sclerosis↗

PubMed2005

Increased production of reactive oxygen species contributes to motor neuron death in a compression mouse model of spinal cord injury.

STUDY DESIGN: Experimental laboratory investigation of the role and pathways of reactive oxygen species (ROS)-mediated motor neuron cell death in a mouse model of compression spinal cord injury. OBJECTIVES: To analyze ROS-mediated oxidative stress propagation and signal transduction leading to motor neuron apoptosis induced by compression spinal cord injury. SETTING: University of Louisville Health Science Center. METHODS: Adult C57BL/6J mice and transgenic mice overexpressing SOD1 were severely lesioned at the lumbar region by compression spinal cord injury approach. Fluorescent oxidation, oxidative response gene expression and oxidative stress damage markers were used to assay spinal cord injury-mediated ROS generation and oxidative stress propagation. Biochemical and immunohistochemical analyses were applied to define the ROS-mediated motor neuron apoptosis resulted from compression spinal cord injury. RESULTS: ROS production was shown to be elevated in the lesioned spinal cord as detected by fluorescent oxidation assays. The early oxidative stress response markers, NF-kappaB transcriptional activation and c-Fos gene expression, were significantly increased after spinal cord injury. Lipid peroxidation and nucleic acid oxidation were also elevated in the lesioned spinal cord and motor neurons. Cytochrome c release, caspase-3 activation and apoptotic cell death were increased in the spinal cord motor neuron cells after spinal cord injury. On the other hand, transgenic mice overexpressing SOD1 showed lower levels of steady-state ROS production and reduction of motor neuron apoptosis compared to that of control mice after spinal cord injury. CONCLUSION: These data together provide direct evidence to demonstrate that the increased production of ROS is an early and likely causal event that contributes to the spinal cord motor neuron death following spinal cord injury. Thus, antioxidants/antioxidant enzyme intervention combined with other therapy may provide an effective approach to alleviate spinal cord injury-induced motor neuron damage and motor dysfunction.

Animals↗

PubMed2004

Identification of the carbon dangling bond center at the 4H-SiC/SiO(2) interface by an EPR study in oxidized porous SiC.

We report the observation of a paramagnetic interface defect in thermally oxidized porous n-type doped 4H-SiC/SiO(2). Based on its axial symmetry and resolved hyperfine interactions it is attributed to an sp(3) carbon dangling bond center situated at the SiC side of the interface. This center is electrically active and pins the Fermi level in the oxidized samples. No silicon related paramagnetic dangling bond centers are observed. The formation of dangling bond centers seems to be related to interstitial oxygen diffusion at the interface during the oxidation process.

Journal Article↗

PubMed2004

Increased oxidative stress is associated with chronic intermittent hypoxia-mediated brain cortical neuronal cell apoptosis in a mouse model of sleep apnea.

Chronic intermittent hypoxia (CIH), as occurs in obstructive sleep apnea (SA), is associated with substantial cortico-hippocampal damage leading to impairments of neurocognitive, respiratory and cardiovascular functions. Previous studies in a rat model have shown that CIH increases brain cortical neuronal cell death. However, the molecular events leading to CIH-mediated neuronal cell death remain largely undefined. The oscillation of O2 concentrations during CIH remarkably mimics the processes of ischemia/re-oxygenation and could therefore increase cellular production of reactive oxygen species (ROS). We extended the CIH paradigm to a mouse model of SA to identify the molecular mechanisms underlying cortical neuronal cell death. A significant increase of ROS production in mouse brain cortex and cortical neuronal cells was detected by fluorescent oxidation assays upon exposure of mice to CIH, followed by increased expression of oxidative stress response markers, c-Fos, c-Jun and NF-kappaB in mouse brain cortex, as revealed by immunohistochemical and LacZ reporter assays respectively. Long-term exposure of mice to CIH increased the levels of protein oxidation, lipid peroxidation and nucleic acid oxidation in mouse brain cortex. Furthermore, exposure of mice to CIH induced caspase-3 activation and increased some cortical neuronal cell apoptosis. On the other hand, transgenic mice overexpressing Cu,Zn-superoxide dismutase exposed to CIH conditions had a lower level of steady-state ROS production and reduced neuronal apoptosis in brain cortex compared with that of normal control mice. Taken together, these findings suggest that the increased ROS production and oxidative stress propagation contribute, at least partially, to CIH-mediated cortical neuronal apoptosis and neurocognitive dysfunction.

Animals↗

PubMed2004

Nanoporous SiC: a candidate semi-permeable material for biomedical applications.

We have fabricated free-standing SiC nanoporous membranes in both p -type and n -type material. We showed that these membranes will permit the diffusion of proteins up to 29000 Daltons, while excluding larger proteins. By using radioactively labeled albumin, we also show that porous SiC has very low protein adsorption, comparable to the best commercially available polymer nanoporous membrane.

Adsorption↗

PubMed2004

Relationship between upregulated oestrogen receptors and expression of growth factors in cultured, human, prostatic stromal cells exposed to estradiol or dihydrotestosterone.

This study investigated the hypothesis that, in benign prostatic hyperplasia (BPH), upregulated oestrogen receptors (ER) and the action of androgens differentially regulate expression of stromal growth factors. Eight human prostatic stromal cell strains were subjected to a procedure to upregulate their ER by exposing them to 1 micromol 17beta-estradiol for 10 days followed by passage and growth in the absence of steroids. Four of the cell strains instead received 100 nmol dihydrotestosterone for 48 h. Immunoexpression of ERalpha, AR and six growth factors was quantified by flow cytometry in each case. Expression of ERalpha was significantly increased in six of eight cell strains. Expressions of six growth factors (FGF-2, FGF-7, IGF-1, TGF-beta1 NGF and e NOS) were elevated but only for FGF-7 was it significant. There was a significant positive correlation between the change in ERalpha and the change in FGF-2 and FGF-7, but not the other growth factors. Exposure to dihydrotestosterone reduced expression of ERalpha and all six growth factors, compared with oestrogen-treated cells but not significantly. It is concluded that upregulated ERalpha in prostatic stroma may have a greater modulating influence on synthesis of certain growth factors than the direct action of androgens and, by enhancing synthesis of FGF-2 and FGF-7, could play a significant role in the development of BPH.

Dihydrotestosterone↗

PubMed2003

Detection of human papillomavirus-16 in ovarian malignancy.

Human papillomavirus is the causal factor for cervical cancer. However, the role of HPV infection in ovarian cancer is unclear. This study aimed to determine the presence of human papillomavirus-16 (HPV-16) in ovarian cancer tissues. Archived human ovarian cancer tissues (N=54 cases, 50 are epithelial cancer, four are nonepithelial cancer) embedded in paraffin blocks were used. Controls are 30 nonmalignant ovarian tissue blocks. In situ hybridisation (ISH) and immunohistochemistry (IHC) were used to detect the presence of HPV-16 and p53 expression. In all, 52 or 36% of the epithelial ovarian tumours detected by ISH or IHC, respectively, were HPV-16 E6 positive. In contrast, only 6.7% of normal ovarian tissues were HPV-16 positive proved by ISH. Human papillomavirus-16 infection was significantly higher in cancer tissues compared to controls with an odds ratio of 16.7 (95% confidence interval [CI]=3.2-71.4, P<0.01). No significant correlation between HPV-16 infection and histological types of cancer was found (P>0.05). p53 gene expression was detected in 42% epithelial ovarian cancers. No correlation between p53 expression and HPV-16 infection was found. The results showed the presence of HPV-16 E6 in ovarian carcinoma, suggesting that HPV infection might play a role in ovarian carcinogenesis.

Adult↗

PubMed2003

Hyperleptinemia precipitates diet-induced obesity in transgenic mice overexpressing leptin.

Transgenic mice overexpressing leptin backcrossed to the C57BL/6J genetic background (LepTg) have a lean phenotype, characterized by a 95% reduction in adipose mass; reduced plasma levels of glucose, triglycerides, insulin, and IGF-1; and a 75% decrease in adipocyte size. High-fat diet treatment for 20 wk revealed that, compared with normal mice, the LepTg mice had an increased susceptibility to diet-induced obesity, as demonstrated by their rate of weight gain, higher accumulation of sc white adipose tissue mass, hypertrophy of adipocytes, and normalization of their reduced metabolic parameters. The stromal vascular fraction of white adipose tissue from the LepTg mice was highly cellular and contained cells capable of rapid lipid accumulation in primary cultures. The precipitous diet-induced obesity of the LepTg mice was accompanied with 10-fold and 1.6-fold elevations in insulin and IGF-1, respectively, suggesting that the trophic action of insulin and IGF-1 on the preadipocytes and small adipocytes may have caused them to rapidly differentiate and accumulate triacylglycerol stores. Other contributing factors may involve a shift in insulin sensitivity triggered by hyperleptinemia and a decrease in energy expenditure. These studies demonstrate that a chronic response to hyperleptinemia as in the LepTg mice is a predisposing factor to diet-induced obesity and suggest that individuals who are particularly lean because of increased leptin secretion may develop rapid obesity under conditions of a high-fat diet.

Adipocytes↗

PubMed2002

Biexponential transverse relaxation (T(2)) of the proton MRS creatine resonance in human brain.

Differences in proton MRS T(2) values for phosphocreatine (PCr) and creatine (Cr) methyl groups (3.0 ppm) were investigated in studies of phantoms and human brain. Results from phantom studies revealed that T(2) of PCr in solution is significantly shorter than T(2) of Cr. Curve-fitting results indicated that the amplitude-TE curves of the total Cr resonance at 3.0 ppm in human brain (N = 26) fit a biexponential decay model significantly better than a monoexponential decay model (P < 0.006), yielding mean T(2) values of 117 +/- 21 ms and 309 +/- 21 ms. Using a localized, long-TE (272 ms) point-resolved spectroscopy (PRESS) proton MRS during 2 min of photic stimulation (PS), an increase of 12.1% +/- 3.5% in the mean intensity of the total Cr resonance in primary visual cortex (VI) was observed at the end of stimulation (P < 0.021). This increase is consistent with the conversion of 26% of PCr in VI to Cr, which is concordant with (31)P MRS findings reported by other investigators. These results suggest a significantly shorter T(2) for PCr than for Cr in vivo. This difference possibly could be exploited to quantify regional activation in functional spectroscopy studies, and could also lead to inaccuracies in some circumstances when the Cr resonance is used as an internal standard for (1)H MRS studies in vivo.

Adult↗

PubMed2002

Prostatic stem cells.

Multipotent cells within the epithelial compartment, together with phenotypically 'plastic' mesenchyma cells (stromal stem cells), provide a repository of protected genetic information from which the structure, stability and functionality of the prostate gland can be maintained. However, mere preservation of cells in a non-dividing state is insufficient to provide the necessary reservoir of information from which the structure and function of the prostate gland can be retained or recreated. Rather, there is a constant dynamic interaction, at the level of information exchange, between stem cells (whether epithelial or mesenchymal) and their surrounding environment (both humoral and physical). Thus, with respect to epithelial stem cells, these reside within environmental 'niches' which allow their controlled and limited proliferation while preserving genomic integrity. Similar 'mesenchymal niches' are also predicted to occur, although not yet identified, thus providing the multipotent source from which the full spectrum of stromal phenotypes might be regenerated. Recent data from studies of the haematopoietic and hepato-biliary systems indicate that the potential scope of stem cells far exceeds the immediate phenotypic complement of those tissues within which they originate, being dependent upon their precise environment as well as their genomic integrity.

Cell Differentiation↗

PubMed2002

Upregulation of estrogen and androgen receptors modulate expression of FGF-2 and FGF-7 in human, cultured, prostatic stromal cells exposed to high concentrations of estradiol.

This study was performed to develop an experimental model in which expression of estrogen receptors (ER) by human prostatic stromal cells could be reproducibly enhanced relative to similar cells with low ER expression. The second aim was to characterise changes in expression of ER, androgen receptor (AR), FGF-2 and FGF-7 in stromal cells exposed to high and low concentrations of estradiol and testosterone mimicking the different sex hormone levels between young and elderly men. Five strains of human prostatic stromal cells, isolated from BPH resections, were grown in steroid-free medium plus 1 micromol 17beta-estradiol. After 10 days, cells were passaged and grown in the same medium without estradiol until confluent. In a second study four cell strains were exposed to high and low concentrations of 17beta-estradiol and testosterone for 10 days. Cells were labelled with fluorescent antibodies to ERalpha, AR, FGF-2 and FGF-7 and the fluorescence intensity measured by flow cytometry. Following exposure to 1 micromol estradiol, stromal cells showed reduced expression of AR and ERalpha but after passage without estradiol they showed a 25% increase in both receptors over controls. Different combinations of sex hormones induced inconsistent changes with respect to expression of ER, AR and FGFs in the various cell-strains. However, there was a highly significant correlation between AR, ER and FGF-2 and FGF-7, which was cell strain-specific. Thus, changes in sex hormone balance per se may not be solely responsible for the observed increases in prostatic ER levels in BPH. Since expression of ER is correlated with synthesis of FGF-2 and FGF-7, it is likely that increases in stromal ER may mediate the synthesis of stromally-derived growth factors which contribute to the aetiopathogenesis of benign prostatic hyperplasia.

Culture Techniques↗

PubMed2001

Human cutaneous fatty acid-binding protein induces metastasis by up-regulating the expression of vascular endothelial growth factor gene in rat Rama 37 model cells.

Human cutaneous fatty acid-binding protein (C-FABP) gene is capable of inducing the metastatic phenotype when overexpressed in nonmetastatic rat Rama 37 cells. However, the mechanism of how it induces metastasis is not clear. Northern and slot blot analyses revealed that expression of the endogenous vascular endothelial growth factor (VEGF) gene was increased by 3.8-5.2-fold in the C-FABP-transfected cells (pSV-CFABP-R37) and in their metastatic sublines (e.g., Met-1) when compared with that in the nonmetastatic control transfectant pSV-R37 cells generated by transfection of only plasmid DNA. Higher levels of VEGF immunoreactive protein were also secreted from the malignant C-FABP-expressing cells. Reverse transcription-PCR detected two VEGF transcript isoforms, VEGF(164) and VEGF(188), in both the nonmetastatic control transfectant pSV-R37 cells and the malignant metastatic Met-1 cells. Chick chorioallantoic membrane assays showed that the conditioned medium of the control pSV-R37 cells possessed only very weak angiogenic activity, whereas conditioned media from the metastatic C-FABP transfectants and their sublines were strongly angiogenic and could be inhibited by antibodies to VEGF. Transfection of VEGF(164) cDNA in an expression vector into nonmetastatic Rama 37 cells produced a cell clone (R37-VEGF-2) that expressed high levels of VEGF. Inoculation of R37-VEGF-2 cells into syngeneic Wistar Furth rats produced metastases in a significant number (Fisher's exact test, P < 0.01) of animals (18 of 31 animals), whereas the control, vector alone-transfected R37-PSV cells produced no metastases (0 of 30 animals). Immunocytochemical methods demonstrated a strong positive staining for VEGF and an increased microvessel density in the primary tumors produced from PSV-VEGF-2 cells in comparison with tumors produced from control transfectants. Immunocytochemical staining for factor VIII detected a 3.5-fold increase in microvessel density of the primary tumors produced by PSV-VEGF-2 cells when compared with that of the primary tumors developed from the control pSV-R37 cells. Therefore, we suggest that overexpression of the C-FABP gene in the original transfectants induces metastasis through up-regulation of expression of the VEGF gene in this rat Rama 37 model system, and thus VEGF may play a crucial role in this particular metastatic cascade.

Animals↗

PubMed2001

African origin of modern humans in East Asia: a tale of 12,000 Y chromosomes.

To test the hypotheses of modern human origin in East Asia, we sampled 12,127 male individuals from 163 populations and typed for three Y chromosome biallelic markers (YAP, M89, and M130). All the individuals carried a mutation at one of the three sites. These three mutations (YAP+, M89T, and M130T) coalesce to another mutation (M168T), which originated in Africa about 35,000 to 89,000 years ago. Therefore, the data do not support even a minimal in situ hominid contribution in the origin of anatomically modern humans in East Asia.

Africa↗

PubMed2001

Exercise decreases cytosolic aconitase activity in the liver, spleen, and bone marrow in rats.

Effects of strenuous exercise on cytosolic aconitase activity (CAA) were investigated in this study. Female Sprague-Dawley rats were randomly assigned to four groups: S1 (Sedentary), S2 (Sedentary + L-NAME [N-nitro-l-arginine methyl ester]), E1 (Exercise), and E2 (Exercise + L-NAME). Rats in the E1 and E2 groups swam for 2 h/day for 3 months. L-NAME (an inhibitor of NOS) in drinking water (1 mg/ml) was administered to rats in the S2 and E2 groups for the same period. At the end of the third month, the CAA in the liver, spleen, and bone marrow cells was measured. In the exercise group (E1), CAA in the liver, spleen, and bone marrow cells was 19.99 +/- 1.49, 1.61 +/- 0.13, and 0.59 +/- 0.09 mU/mg protein, respectively. These values were significantly lower than the corresponding sedentary values in the S1 group (33.96 +/- 1.38, 3.96 +/- 0.19, and 3.20 +/- 0.18 mU/mg protein) (P < 0.01, 0.001, and 0.001, respectively). The treatment of L-NAME led to a significant increase in tissue CAA in the sedentary rats (S2). Also, the significantly higher CAA in the liver, spleen, and bone marrow cells was found in the exercised rats treated with L-NAME (E2) (29.50 +/- 1.27, 2.89 +/- 0.25, and 1.34 +/- 0.20 mU/mg) than without L-NAME (E1) (P < 0.01, 0.01, 0.05, respectively). However, the values in the E2 group were still significantly lower than those in the S1 group (P < 0.05, 0.01, and 0.001, respectively). This indicates that L-NAME treatment can partly recover the decreased CA in tissues in the exercised rats. These results provide evidence for the existence of the increased activity of IRP1 (iron regulatory protein 1) that is probably induced by the increased nitric oxide production in the strenuously exercised rats.

Aconitate Hydratase↗

PubMed2001

Ceruloplasmin promotes iron uptake rather than release in BT325 cells.

This study was initiated to investigate the mechanism of ceruloplasmin (CP)-mediated iron release from brain cells using BT325 cells (a glioblastoma cell line); however, negative results were obtained. The BT325 cells were preloaded with 1 microM 59Fe2+ in sucrose (pH 5.8) for 60 min, and then with CP (0-300 microg/ml) for 30 min at 37 degrees C. The addition of CP, either at low (25 microg/ml) or high (300 microg/ml) concentrations, did not lead to a significant change in iron release from iron-loaded BT325 cells. No significant difference in total iron of cells was found between all CP treated groups and the control (P>0.05). Although apotransferrin (apoTf) was shown to have a role in iron release from the cells, the effect of apoTf was not significantly affected by the addition of different concentrations of CP. When the cells were incubated with 1 microM 59Fe2+ in the presence of varying amounts of CP for 30 min at 37 degrees C, it was found that CP increased iron uptake. The total iron uptake by BT325 cells in CP treatment groups (25, 75, 150, 300 microg/ml) was significantly higher than that in the control (no CP addition) (all P<0.01). Furthermore, in contrast to our expectation, CP was shown to promote significantly iron uptake in not only iron-sufficient but also iron-deficient cells. These results showed that CP had a role in iron uptake rather than release in BT325 cells.

Animals↗

PubMed2001

Rethinking the role of ceruloplasmin in brain iron metabolism.

For more than three decades, it has been widely accepted that ceruloplasmin plays an important role in iron efflux from mammalian cells, including brain cells, via the activity of ferroxidase. However, in light of recent findings, this view might not be completely accurate and the role of ceruloplasmin in brain iron metabolism may need to be re-evaluated. Based on recent studies, we propose in this article that the role of ceruloplasmin in iron uptake by brain neuronal cells might be more important than its role in iron release from the cells. A possible explanation of why the absence of ceruloplasmin induces excessive iron accumulation in neurons in aceruloplasminemia (ceruloplasmin gene mutations) was also discussed.

Animals↗

PubMed2001

Human papillomavirus type 16 is an important infectious factor in the high incidence of esophageal cancer in Anyang area of China.

To investigate the potential role of human papillomavirus (HPV) infection in the pathogenesis of esophageal carcinomas in the Anyang area of China, we have evaluated specimens collected by balloon cytology examination from volunteers in two regions with significantly different incidences of esophageal carcinoma. 138 donors were from a village in a county with an esophageal carcinoma (EC) age-adjusted mortality rate of 132x10(5), the remaining 68 were resident in a second village from another county with an EC mortality rate of 52x10(5). Specimens were evaluated using both polymerase chain reaction (PCR) amplification and in situ hybridization (ISH) protocols. PCR results showed that the prevalence of the human papillomavirus type 16 (HPV-16) E6 gene in the high incidence area was 1.9-fold higher than that of the low incidence area (72 and 37%, respectively, P < 0.01). Moreover, the positive rate corresponded with pathology grade. Similar results were obtained with the HPV-16 E7 gene. As the cells undergoing cytopathological progress, the HPV-16 E6 positive rate was increased, in both villages. In contrast to HPV-16 E6 and E7, detection of the HPV L1 gene was consistently lower, and its prevalence decreased with increasing dysplasia grades (P < 0.05). By ISH analyses, the expression rate of HPV-16 E6 in the specimens collected from the high incidence area was 2.2-fold higher than those from the low incidence area (49 versus 22%, respectively; P < 0.05), and transcription of the E6 gene paralleled cytopathology. HPV-18 was also detected in 17 and 15% of the specimens from the high and low incidence areas, respectively, but most of these samples were also simultaneously HVP-16 positive. These results suggest that HVP-16 plays a causative role in the high incidence of esophageal cancer in the Anyang region of CHINA:

China↗

PubMed2001

Increased nitric oxide is one of the causes of changes of iron metabolism in strenuously exercised rats.

This study was carried out to investigate the possible role of increased nitric oxide (NO) production in the development of the low iron status in strenuously exercised rats. Female Sprague-Dawley rats were randomly assigned to four groups: sedentary (S1), sedentary + nitro-L-arginine methyl ester (L-NAME; S2), exercise (E1), and exercise + L-NAME (E2). Animals in the E1 and E2 groups swam for 2 h/day for 3 mo. L-NAME in the drinking water (1 mg/ml) was administrated to rats in the S2 and E2 groups for the same period. At the end of third month, hematological indexes and nitrite and nitrate (NOx) contents in the plasma and non-heme iron and NOx levels in the liver, spleen, and bone marrow cells were measured. Three months of exercise induced a significant increase in NOx content and a decrease in iron level both in plasma and tissues. Treatment with L-NAME, an inhibitor of NO synthase (NOS), led to a significant decrease in NOx and an increase in iron level both in plasma and tissues in the exercised rats. The E2 group had a significantly lower NOx content as well as a higher iron level both in plasma and tissues than the E1 group. However, the iron contents in the plasma and tissues of the E2 group were still significantly lower than those found in S1. No difference was found in NOx levels between E2 and S1. These findings showed that exercise was associated with elevation in NOx and reduction in iron in plasma and the tissues. Treatment with L-NAME was able to completely inhibit the effect of exercise on NOx as well as partly recover the decreased iron contents in plasma and tissues resulting from exercise. This suggests that the increased production of NO might be one of the causes of the lower iron status in exercised rats.

Animals↗