In silico and in vivo protective effect of Morus nigra leaves on oxidative damage induced by iron overload.

Morus nigra L. is a plant popularly known as 'amoreira preta', very used in folk medicine. Iron overload (hemochromatosis) is a clinical condition that causes damage to various tissues due to oxidative stress. Therapy to control iron overload is still unsatisfactory. The protective effect on oxidative stress induced by iron overload was verified. Phytochemical characterization was evaluated by UHPLC-MS/MS. The in silico toxicity predictions of the main phytochemicals were performed via computer simulation. To induce iron overload, the animals received iron dextran (50 mg/kg/day). The test groups received doses of 500 and 1000 mg/kg of M. nigra extract for six weeks. Body weight, organosomatic index, serum iron, hepatic markers, cytokines, interfering factors in iron metabolism, enzymatic and histopathological evaluations were analyzed. Vanillic acid, caffeic acid, 6-hydroxycoumarin, p-coumaric acid, ferulic acid, rutin, quercitrin, resveratrol, apigenin and kaempferol were identified in the extract. In addition, in silico toxic predictions showed that the main compounds presented a low probability of toxic risk. The extract of M. nigra showed to control the mediators of inflammation and to reduce iron overload in several tissues. Our findings illustrate a novel therapeutic action of M. nigra leaves on hemochromatosis caused by iron overload.

Polymorphism eNOS Glu298Asp modulates the inflammatory response of human peripheral blood mononuclear cells.

INTRODUCTION: Nitric oxide is a gaseous radical produced by the nitric oxide endothelial synthase (eNOS) whose most studied physiological action is the vasodilation. However, it also acts in the defense of the organism through the formation of cytotoxic radicals, which can potentiate the inflammatory lesion of the cells. The Glu298Asp is a single nucleotide polymorphism (SNP) in the eNOS gene related to the risk of cardiovascular disease. Blacks present a higher prevalence of hypertension and cardiovascular mortality. Then, we aimed to evaluate the influence of Glu298Asp polymorphism on inflammatory response in vitro and gene expression in blacks. MATERIAL AND METHODS: Peripheral blood mononuclear cells (PBMC) from blacks with different Glu298Asp genotypes were treated with phytohemagglutinin (PHA), a mitogen and activator of T cells. Oxidative, inflammatory markers, and expression of inflammation genes were evaluated. RESULTS: The genotype frequencies were TT 6.7%; TG 29.3% and GG 64.0%. Activation of PBMCs with 125 µg of PHA modulated the expression of inflammatory genes and increased levels of inflammatory cytokines. The T allele showed increased susceptibility to inflammation (higher levels of interleukin 1, interleukin 6 and tumor necrosis factor alpha; p < 0.001). The G allele exhibited protection through higher levels of nitric oxide (p < 0.001) and fewer inflammatory cytokines. CONCLUSION: Despite methodological limitations related to in vitro assays, the whole of results suggested that Glu298Asp modulates inflammatory genes, the T allele is more susceptible to inflammation and the G allele is protective.

Spinal cord injury by clip-compression induces anxiety and depression-like behaviours in female rats: The role of the inflammatory response.

Traumatic spinal cord injury (SCI) promotes long-term disability that affects mobility and functional independence. The spinal cord inflammatory response after the initial mechanical insult substantially impacts locomotor impairment and development of neuropsychiatric disorders, including anxiety and depression. However, these psychiatric events are scarcely investigated in females. This study investigated the anxiety/depression-like behaviours and inflammatory responses related to the production/release of pro- and anti-inflammatory cytokines in female adult Wistar rats submitted to severe clip-compression SCI. Data showed that SCI impaired the locomotor performance assessment by the BBB scale, but did not alter exploratory activity in open-field test. Animals' locomotor impairment was associated with anxious and depressive-like behaviours characterised by a decreased amount of time in the open arms of the elevated plus-maze test, and the motivational reduction of social interaction and anhedonia assessed by social exploration and sucrose preference tests. By contrast, SCI decreased the immobility time in the forced swimming test. Moreover, SCI caused a significant increase in local and systemic proinflammatory cytokines (TNF-α, INF-γ, IL-1ß, and IL-6) and a reduction in the anti-inflammatory cytokine IL-10. Finally, there were significant negative correlations between depression-like behaviour, but not anxiety, and increased plasma concentrations of TNF-α, IL-1ß, IL-6, and INF-γ. Additionally, the laminectomy procedure provoked the inflammatory response associated with reduced sucrose intake in Sham animals, although less expressively than in the SCI group. Collectively, these results indicate that SCI by clip-compression in female rats promotes a neuropsychiatric-like profile associated with an imbalance in the production/release of pro- and anti-inflammatory cytokines.

Immunomodulatory effect of mancozeb, chlorothalonil, and thiophanate methyl pesticides on macrophage cells.

Mancozeb (MZ), chlorothalonil (CT), and thiophanate methyl (TM) are pesticides commonly used in agriculture due to their efficacy, low acute toxicity to mammals, and short environmental persistence. Although the toxic effects of these pesticides have been previously reported, studies regarding their influence on the immune system are limited. As such, this study focused on the immunomodulatory effect of MZ, CT, and TM pesticides on macrophage cells. RAW 264.7 cells were exposed to a range of concentrations (0.1-100 µg/mL) of these pesticides. CT exposure promoted an increase in reactive oxygen species (ROS) and nitric oxide (NO) levels. The MTT and ds-DNA assay results demonstrated that MZ, CT, and TM exposure induced macrophage proliferation. Moreover, MZ, CT, and TM promoted cell cycle arrest at S phase, strongly suggesting macrophage proliferation. The levels of pro-inflammatory cytokines (IL-1ß, IL-6, TNF-α, and IFN-γ) and caspases (caspase 1, 3, and 8) in macrophages exposed to MZ, CT, and TM pesticides increased, whereas the anti-inflammatory cytokine levels decreased. These results suggest that MZ, CT, and TM exert an immunomodulatory effect on the immune system, inducing macrophage activation and enhancing the inflammatory response.

In vitro effect of low-level laser therapy on the proliferative, apoptosis modulation, and oxi-inflammatory markers of premature-senescent hydrogen peroxide-induced dermal fibroblasts.

Skin aging is a complex biological process induced by intrinsic and extrinsic factors which is characterized by clinical and cellular changes, especially dermal fibroblasts. It is possible that, some procedures, such as low-level laser therapy (LLLT), could decelerate this process. To test this hypothesis, this study evaluated the in vitro LLLT on dermal fibroblast cell line (HFF-1) with premature senescence H2O2-induced. HFF-1 cells were cultured in standardized conditions, and initially H2O2 exposed at different concentrations. Fibroblasts were also just exposed at different LLLT (660 nm) doses. From these curves, the lowest H2O2 concentration that induced indicators of premature senescence and the lowest LLLT doses that triggered fibroblast proliferation were used in all assays. Cellular mortality, proliferation, and the levels of oxidative, inflammatory cytokines, apoptotic markers, and of two growth signaling molecules (FGF-1 and KGF) were compared among treatments. The H2O2 at 50 µM concentration induced some fibroblast senescence markers and for LLLT, the best dose for treatment was 4 J (p < 0.001). The interaction between H2O2 at 50 µM and LLLT at 4 J showed partially reversion of the higher levels of DNA oxidation, CASP 3, CASP 8, IL-1B, IL-6, and INFy induced by H2O2 exposure. LLLT also trigger increase of IL-10 anti-inflammatory cytokine, FGF-1 and KGF levels. Cellular proliferation was also improved when fibroblasts treated with H2O2 were exposed to LLLT (p < 0.001). These results suggest that in fibroblast with some senescence characteristics H2O2-induced, the LLLT presented an important protective and proliferative action, reverting partially or totally negative effects triggering by H2O2.

Ziprasidone, a second-generation antipsychotic drug, triggers a macrophage inflammatory response in vitro.

Antipsychotic drugs are used to treat schizophrenia and other psychiatric disorders. However, most of these drugs present side effects causing obesity and other serious metabolic alterations that correlate with grade of chronic inflammation. In contrast, ziprasidone's (ZIP) metabolic side effects are attenuated relative to those of other antipsychotic drugs, but some reports suggest that this drug could cause allergic, hypersensitive reactions in susceptible patients. At present, the mechanism of ZIP's effect on peripheral inflammatory metabolism is not well characterized. We conducted an in vitro study to evaluate the effect of ZIP on a macrophage cell line (RAW 264.1). Our results showed that in non-activated macrophage cells, ZIP exposure initiated macrophage spreading; increased cellular proliferation, as evaluated by MTT and flow cytometry assays; and presented higher levels of oxidant molecules involved in the inflammatory response (nitric oxide, superoxide, reactive oxygen species), and proinflammatory cytokines (IL-1, IL-6, TNFα, INFγ). Levels of IL-10, an anti-inflammatory cytokine were lower in ZIP-exposed cells. These effects were less potent than those caused by the positive control for inflammation induction (phytohemagglutinin), and more intense than the effects of lithium (LI), which was used as an anti-inflammatory molecule. ZIP also modulated cytokine gene expression. Taken together, these data suggest that ZIP can produce a peripheral inflammatory response, and this response may explain the allergen-inflammatory response observed in some patients treated with this antipsychotic drug.

Effect of atorvastatin on behavioral alterations and neuroinflammation during epileptogenesis.

Temporal lobe epilepsy (TLE) is the most frequent and medically refractory type of epilepsy in humans. In addition to seizures, patients with TLE suffer from behavioral alterations and cognitive deficits. Poststatus epilepticus model of TLE induced by pilocarpine in rodents has enhanced the understanding of the processes leading to epilepsy and thus, of potential targets for antiepileptogenic therapies. Clinical and experimental evidence suggests that inflammatory processes in the brain may critically contribute to epileptogenesis. Statins are inhibitors of cholesterol synthesis, and present pleiotropic effects that include antiinflammatory properties. We aimed the present study to test the hypothesis that atorvastatin prevents behavioral alterations and proinflammatory state in the early period after pilocarpine-induced status epilepticus. Male and female C57BL/6 mice were subjected to status epilepticus induced by pilocarpine and treated with atorvastatin (10 or 100mg/kg) for 14days. Atorvastatin slightly improved the performance of mice in the open-field and object recognition tests. In addition, atorvastatin dose-dependently decreased basal and status epilepticus-induced levels of interleukin-1ß (IL-1ß), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (INF-γ) and increased interleukin-10 (IL-10) levels in the hippocampus and cerebral cortex. The antiinflammatory effects of atorvastatin were qualitatively identical in both sexes. Altogether, these findings extend the range of beneficial actions of atorvastatin and indicate that its antiinflammatory effects may be useful after an epileptogenic insult.

Impact of Lipid-Inflammatory-Oxidative Metabolism on Auditory Skills after Hearing Aid Fitting in the Elderly.

This study aimed to assess whether lipid-inflammatory-oxidative metabolism influences auditory processing skills, and whether they function in changing auditory performance after hearing aid fitting in the elderly. Twelve subjects with bilateral hearing loss were submitted to blood tests (to check their lipid-inflammatory-oxidative metabolism) and auditory processing skill tests. After 3 months of using the hearing aids, their auditory skills were re-evaluated and the data were correlated statistically. Oxidative stress levels mainly showed some impact on auditory temporal processing; such a relation and others should best be examined in further studies with larger populations.

The anti-inflammatory effects of resveratrol on human peripheral blood mononuclear cells are influenced by a superoxide dismutase 2 gene polymorphism.

Resveratrol is an molecule that provides both anti-inflammatory and antioxidant properties. However, it is unclear whether the basal oxidative state of the cell has any influence on the effects of this compound. In humans, a single nucleotide polymorphism (SNP) is present in the enzyme manganese superoxide dismutase (SOD2), localized in codon 16 (rs4880), which can either be an alanine (A) or valine (V). This SNP causes an imbalance in the cellular levels of SOD2, where AA- and VV-genotypes result in higher or lower enzymatic activity, respectively. Furthermore, the VV-genotype has been associated with high levels of inflammatory cytokines. Here, we examined the effects of a range of resveratrol concentrations on the in vitro activation of human peripheral blood mononuclear cells (PBMCs) carrying different Ala16Val-SOD2 genotypes. Cell proliferation, several oxidative biomarkers and cytokines (IL-1ß, IL-6, TNFα, Igγ and IL-10) were analyzed. In addition, the effects of resveratrol on the expression of the sirt1 gene were evaluated by qRT-PCR. After 24 h exposure to resveratrol, A-genotype PBMCs displayed a decrease in cell proliferation, whilst VV-cells contrasted; At 10 µM resveratrol, there was a significant decrease in the production of inflammatory cytokines in A-allele cells; however, VV-cells generally displayed a subtle decrease in these, except for TNFα, which was not affected. In all SOD2 genotypes cells exposed to resveratrol resulted in an upregulation of Sirt1 levels. Together, these results suggest that the effect of resveratrol on human PBMC activation is not universal and is dependent on the Ala16Val-SOD2 SNP.

Evaluation of acetylcholinesterase and adenosine deaminase activities in brain and erythrocytes and proinflammatory cytokine levels in rats submitted to neonatal hypoxia-ischemia model.

Perinatal hypoxic-ischemic (HI) brain injury is a common problem with severe neurologic sequelae. The definitive brain injury is a consequence of pathophysiological mechanisms that begin at the moment of HI insult and may extend for days or weeks. In this context, the inflammatory response and the formation of reactive oxygen species seem to play a key role during evolution of brain damage after injury. Thus, the aim of this study was to describe the chronological sequence of acetylcholinesterase (AChE) activity and the lipid peroxidation changes in the cerebral cortex using the classic model of neonatal HI. Furthermore, the erythrocyte AChE and adenosine deaminase (ADA) activities as well as the serum levels of proinflammatory cytokines were assessed. We observed that neonatal HI caused an increase of lipid peroxidation immediately after HI insult, which remained for several days afterward. There was a time-related change in the AChE activity in the cerebral cortex and the same was observed in erythrocyte AChE and ADA activities. In addition, immediately after HI, ADA activity showed a strong positive correlation with all proinflammatory cytokines assessed. Together, these findings may help the understanding of some mechanism related to the pathophysiology of neonatal HI, therefore highlighting the putative therapeutic targets to minimize brain injury and enhance recovery.

Influence of Toxoplasma gondii acute infection on cholinesterase activities of Wistar rats.

Several studies have shown the mechanisms and importance of immune responses against Toxoplasma gondii infection and the notable role of cholinesterases in inflammatory reactions. However, the association between those factors has not yet been investigated. Therefore, the aim of this study was to evaluate the acetylcholinesterase (AChE) activity in blood and lymphocytes and the activity of butyrylcholinesterase (BChE) in serum of rats experimentally infected with T. gondii during the acute phase of infection. For that, an in vivo study was performed with evaluations of AChE and BChE activities on days 5 and 10 post-infection (PI). The activity of AChE in blood was increased on day 5 PI, while in lymphocytes its activity was enhanced on days 5 and 10 PI (P<0.05). No significant difference was observed between groups regarding to the activity of BChE in serum. A positive (P<0.01) correlation was observed between AChE activity and number of lymphocytes. The role of AChE as an inflammatory marker is well known in different pathologies; thus, our results lead to the hypothesis that AChE has an important role in modulation of early immune responses against T. gondii infection.

A coffee enriched with guarana, selenium, and l-carnitine (GSC) has nutrigenomic effects on oxi-inflammatory markers of relapsing-remitting multiple sclerosis patients: A pilot study.

Relapsing-remitting multiple sclerosis (RRMS) is the most common clinical course of multiple sclerosis (MS), characterized by a chronic inflammatory state and elevated levels of oxidative markers. Food supplements with potential anti-inflammatory, antioxidant and neuroprotective effects have been tested as possible adjuvants in the treatment of MS. In this sense, this pilot study was carried out with the aim of verifying whether a minimum daily dose of a guarana, selenium and l-carnitine (GSC) based multi supplement, mixed in cappuccino-type coffee, administered for 12 weeks to 28 patients with RRMS could differentially modulate oxidative blood markers (lipoperoxidation, protein carbonylation and DNA oxidation) and inflammatory blood markers (protein levels of cytokines IL-1ß, IL-6, TNF-α, IFN-γ, IL-10, gene expression of these cytokines, and NLRP3 and CASP-1 molecules, and C-reactive protein levels). The results indicate that a low concentration of GSC is capable of decreasing the plasma levels of oxidized DNA and pro-inflammatory cytokines of RRMS patients. The results support further research into the action of GSC on clinical symptoms, not only in patients with MS, but also with other neurological conditions.

Inflammatory cytokines in vitro production are associated with Ala16Val superoxide dismutase gene polymorphism of peripheral blood mononuclear cells.

Obesity is considered a chronic low-grade inflammatory state associated with a chronic oxidative stress caused by superoxide production (O(2)(-)). The superoxide dismutase manganese dependent (SOD2) catalyzes O(2)(-) in H(2)O(2) into mitochondria and is encoded by a single gene that presents a common polymorphism that results in the replacement of alanine (A) with a valine (V) in the 16 codon. This polymorphism has been implicated in a decreased efficiency of SOD2 transport into targeted mitochondria in V allele carriers. Previous studies described an association between VV genotype and metabolic diseases, including obesity and diabetes. However, the causal mechanisms to explain this association need to be more elucidated. We postulated that the polymorphism could influence the inflammatory response. To test our hypothesis, we evaluated the in vitro cytokines production by human peripheral blood mononuclear cells (PBMCs) carrier's different Ala16Val-SOD2 genotypes (IL-1, IL-6, IL-10, TNF-α, IFN-γ). Additionally, we evaluated if the culture medium glucose, enriched insulin, could influence the cytokine production. Higher levels of proinflammatory cytokines were observed in VV-PBMCs when compared to AA-PBMCs. However, the culture medium glucose and enriched insulin did not affect cytokine production. The results suggest that Ala16Val-SOD2 gene polymorphism could trigger the PBMCs proinflammatory cytokines level. However, discerning if a similar mechanism occurs in fat cells is an open question.

Vitamin E decreased the activity of acetylcholinesterase and level of lipid peroxidation in brain of rats exposed to aged and diluted sidestream smoke.

INTRODUCTION: The biological systems of both smoker and passive smoking suffer changes caused by toxic compounds from cigarette smoke such as inflammation, lipid peroxidation, and deficiency of vitamin E. The aim of the present study was to evaluate the effect of vitamin E on acetylcholinesterase (AChE) activity and the lipid peroxidation level in the brain of rats in the model of exposure to aged and diluted sidestream smoke (ADSS). METHODS: Adult male Wistar rats (200-300 g) were exposed to ADSS for 4 weeks and treated with vitamin E (50 mg/kg/day) loaded by gavage. In the first, second, third, and fourth weeks, animals were concomitantly exposed to the smoke of 1, 2, 3, and 4 cigarettes/day, respectively. The duration of each exposure was 15 min, daily. RESULTS: For rats exposed to ADSS, the AChE activity and lipid peroxidation level increased in the striatum, cerebral cortex, and cerebellum. In contrast, the activity of AChE and the level of lipid peroxidation decreased in the smoke group treated with vitamin E. CONCLUSIONS: The results suggest that the rats exposed to ADSS and treated with vitamin E significantly reduced the raised activity of AChE and level lipid peroxidation from the brain structures studied. The study, therefore, concludes that vitamin E could be considered as a therapeutic agent in this type of exposure.

Aerobic exercise improves postprandial inflammatory and hemostatic markers after a high-fat meal: a randomized crossover study.

Exercise intensity modulates postprandial lipemia. However, its effect on hemostatic and pro- and anti-inflammatory markers in the postprandial state is still unknown. Eleven young males performed a 2-day trial on different conditions: (i) REST: rest for 45 min; (ii) MIE: moderate-intensity exercise; and (iii) HIE: heavy-intensity exercise. Experimental conditions were performed in the evening. On the following morning, blood samples were taken in the fasted state (0 h) and at 1, 3, and 5 h after the consumption of a high-fat meal (HFM). Interleukin-10 (IL-10) levels were higher in the HIE vs. MIE trial at 0 and 1 h (p < 0.033) and IL-10 incremental area under the curve (iAUC) was greater in the MIE (p = 0.027) and HIE (p = 0.045) trials vs. REST. Lower levels of anti-coagulation factor VII (FVII) were observed at 1 h in the MIE condition vs. REST (p = 0.043). In comparison with REST, MIE improved hemostatic (FVII) and anti-inflammatory markers (IL-10 iAUC) whereas HIE enhanced IL-10 in the postprandial state. Regardless of the exercise intensity, aerobic exercise mitigates the deleterious consequences of an HFM. Novelty: Prior aerobic exercise at moderate-intensity attenuates next day's postprandial FVII and IL-10 levels whereas exercise performed at heavy-intensity increases IL-10 levels. Moderate-intensity exercise may be more beneficial to improve hemostatic (FVII) and anti-inflammatory (IL-10) responses while heavy-intensity exercise may improve anti-inflammatory (IL-10) levels only.

Avocado oil (Persea americana) protects SH-SY5Y cells against cytotoxicity triggered by cortisol by the modulation of BDNF, oxidative stress, and apoptosis molecules.

Chronic psycho-environmental stress can induce neurological dysfunction due to an increase in cortisol levels. It is possible that some food supplements could attenuate its negative impact, such as avocado oil (AO), which is rich in fatty acids with beneficial effects on the brain. This hypothesis was tested by an in vitro model using undifferentiated neuroblastoma cells (SH-SY5Y) exposed to hydrocortisone (HC), an active cortisol molecule with and without AO-supplementation. Cortisol can induce oxidative stress, apoptosis events, and a lowering effect on brain-derived neurotrophic factor (BDNF), a neurogenic molecule. As AO protective effects on HC-exposed cells could involve these routes, some markers of these routes were compared among neuroblastoma cultures. In the first assay, the range concentrations of HC exposure that trigger cell mortality and range AO-concentrations that could revert the HC effect. AO at all concentrations tested (2-30 µg/ml) did not present a cytotoxic effect on SH-SY5Y cells, whereas HC at 0.3-10 ng/ml had a dose-dependent cytotoxic effect on these cells. From these results, HC at 10 ng/ml and AO at 5 µg/ml were chosen for mechanistic analysis. AO was able to decrease the oxidative molecules; however, both AO- and HC-induced differential and varied gene expression modulation of these enzymes. AO partially reverted the protein and gene expression of apoptotic markers that were higher in HC-exposed cells. AO also increases the BDNF levels, which are lower HC-exposed cultures. The results indicate that AO could be a beneficial supplement in situations where cortisol levels are elevated, including chronic psycho-environmental stress. PRACTICAL APPLICATIONS: Psychological chronic stress that induces high cortisol exposure has been linked to premature aging and decreased healthy life expectancy. Neurobiological models involving cortisol have suggested a neurotoxic effect of this molecule, increasing the risk of psychiatric and other CNTDs. This effect can have a high impact mainly in infants and elderly people. In child abuse situations, chronic cortisol exposure could induce extensive apoptosis events, causing impairment in synaptogenesis. In both age groups, chronic cortisol exposure increased the risk of psychiatric conditions, especially anxiety and major depression. However, it is possible that the negative effects associated with chronic cortisol exposure could be attenuated by some food supplements. This is the case for molecules acquired through diet, such as polyunsaturated fatty acids (PUFAs), including omega-3. As inadequate omega-3 levels in the brain can increase the risk factor for neuropsychiatric disorders, it is possible to infer that some from food supplements, such as avocado oil, could attenuate the neurotoxic effects of chronic cortisol exposure. This hypothesis was tested using an exploratory in vitro protocol, and the results suggested that avocado oil could be used as a cytoprotective food supplement by decreasing the oxidative stress and apoptotic events induced by cortisol.

DNA damage and inflammatory response in workers exposed to fuels and paints.

Workers exposed to fuels and paints may present alterations in several parameters. Thus, we assessed potential biomarkers, with the aim of detecting early changes in gasoline station attendants and painters. Blood samples were collected for the analysis of inflammatory and DNA damage markers, besides biochemical, haematological and oxidative stress parameters. Biochemical and haematological parameters, which are assessed with routine exams, showed few changes. However, these findings could mask the workers' real health status. Besides, markers of oxidative damage were not modified. Levels of inflammatory parameters (cytokines and nitric oxide levels) and the DNA damage marker 8-hydroxydeoxyguanosine were significantly changed in the workers. Our results suggest that inflammatory and DNA damage parameters can be potential biomarkers for the biological monitoring of workers exposed to fuels and paints and may contribute to the development of occupational protection standards.

Characteristics of a nickel-albumin binding assay for assessment of myocardial ischaemia.

BACKGROUND: The aim of this study was to describe a method to measure ischaemia-induced alterations of the binding capacity of serum albumin to exogenous nickel. METHODS: We measured the levels of cardiac troponin I (cTnI), serum albumin, ischaemia-modified albumin (IMA) measured by a cobalt-albumin binding assay (CABA), and a nickel-albumin binding assay (NABA) in the following groups: myocardial infarction (n = 32) and non-ischaemic chest pain (n = 64). RESULTS: IMA, cTnI and NABA levels were higher in the myocardial infarction group. NABA presented a higher ability to discriminate myocardial ischaemia than CABA. CONCLUSIONS: Patients with myocardial infarction have reduced nickel binding to human serum albumin, and NABA may have an important role as an early marker of myocardial ischaemia.

Association between thyroid hormones, lipids and oxidative stress biomarkers in overt hypothyroidism.

BACKGROUND: The aim of this study was to investigate the effect of hypothyroidism on lipid peroxidation and the antioxidant profile, as well as to evaluate the interaction between thyroid hormones and biomarkers of oxidative stress in patients with overt hypothyroidism. We also evaluated the influence of cholesterol concentrations on biomarkers of oxidative stress in these same patients. METHODS: Total cholesterol (TC), high-density lipoprotein (HDL) cholesterol, low-density lipoprotein (LDL) cholesterol, triglycerides, thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase (CAT), and vitamin E were measured in 20 subjects with overt hypothyroidism (OH) and 20 controls. RESULTS: TC, LDL cholesterol, triglycerides, TBARS, SOD, CAT, and vitamin E were significantly higher in the OH group. Significant correlation was observed for TSH and SOD, CAT, vitamin E and TBARS. Correlation was observed for triiodothyronine (T3) and SOD, CAT, vitamin E and TBARS. Significant correlation was also observed for free thyroxine and vitamin E and TBARS. However, correlation between T3 and CAT remained significant after controlling for TC concentrations. CONCLUSIONS: Overt hypothyroidism is associated with an increase in oxidative stress, and hypercholesterolemia has a stronger influence on development of oxidative stress in hypothyroid conditions compared with thyroid hormones.