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The objective of this study is to investigate the relationship between altered plasma trace elements, particularly selenium (Se), with Hyper-homocysteinemia (HhCys) as a predictive factor of insulin secretion dysfunction. The study is carried out on adult Psammomys obesus, divided in 4 experimental groups: (I) Normoglycemic/Normoinsulinemic; (II) Normoglycemic/Hyperinsulinemic; (III) Hyperglycaemic/Hyperinsulinemic and (IV) Hyperglycaemic/Insulin deficiency with ketoacidosis. The data showed that a drastic depletion of Se plasma levels is positively correlated with HhCys (>15 µmol/L; p <.001), concomitantly with decreased GPx activity, GSH levels, and GSH/GSSG ratio in group IV both in plasma and liver. In contrast, SOD activity is increased (p ≤.001) in group IV both in plasma and liver. However, plasma Cu and Mn levels increased, while plasma Zn levels decreased in group IV (p <.001). Our study confirms the increase of plasma hCys levels seemed to be a major contributing factor to antioxidant capacities and alters the availability of selenium metabolism by interference with homocysteine synthesis in the insulin secretion deficiency stage. [ABSTRACT FROM AUTHOR]

Objective: To explore the predictive value of serum hyperhomocysteine(Hcy), uric acid(UA) and cystatin C(Cyst-C)levels in the occurrence of carotid atherosclerosis in patients with H type hypertension. Methods: A total of 163 patients with H type hypertension, who were admitted to Chongqing Zhongshan Hospital from May 2014 to May 2015, were chosen as research subjects and divided into normal carotid intima-media thickness(c IMT) group(n=51), thickened c IMT group(n=54) and carotid artery plaque group(n=58) according to the difference of c IMT. The gender, age, serum Hcy, Cyst-C, UA, blood glucose(GLU), blood lipid, blood urea nitrogen(Bun) and serum creatinine(Scr) levels among the three groups are detected and compared, and their correlation with c IMT was analyzed. The influencing factors of carotid atherosclerosis were analyzed by logistic regression analysis. Results: There were significant differences in the HDL-C, Hcy, Cyst-C and UA levels among the three groups(P<0.05). c IMT was positively correlated with the serum Hcy, Cyst-C and UA(r=0.23, 0.32, 0.30; P<0.05), negatively correlated with HDL-C(r=-0.410, P<0.05). Logistic regression analysis showed that the levels of Hcy, Cyst-C and UA were the risk factors of carotid atherosclerosis(OR=1.203, 6.395, 1.023; P<0.05).Conclusion: Serum Hcy, Cyst-C and UA levels are positively correlated with c IMT in the patients with H type hypertension. They are the independent risk factors leading to carotid atherosclerosis,which can be used to predict the occurrence and development of atherosclerosis in the early stage in clinic. [ABSTRACT FROM AUTHOR]

Homocysteine, a sulfur-containing amino acid derived from the methionine metabolism, is located at the branch point of two pathways of the methionine cycle, i.e. remethylation and transsulfuration. Gene abnormalities in the enzymes catalyzing reactions in both pathways lead to hyperhomocysteinemia. Hyperhomocysteinemia is associated with increased risk for congenital disorders, including neural tube closure defects, heart defects, cleft lip/palate, Down syndrome, and multi-system abnormalities in adults. Since hyperhomocysteinemia is known to affect the extent of DNA methylation, it is likely that abnormal DNA methylation during embryogenesis, may be a pathogenic factor for these congenital disorders. In this review we highlight the importance of homocysteinemia by describing the genes encoding for enzymes of homocysteine metabolism relevant to the clinical practice, especially cystathionine-β-synthase and methylenetetrahydrofolate reductase mutations , and the impairment of related metabolites levels. Moreover, a possible correlation between hyperhomocysteine and congenital disorders through the involvement of abnormal DNA methylation during embryogenesis is discussed. Finally, the relevance of present and future diagnostic tools such as tandem mass spectrometry and next generation sequencing in newborn screening is highlighted. [ABSTRACT FROM AUTHOR]

Abstract: Recent evidence suggests that children with autism have impaired detoxification capacity and may suffer from chronic oxidative stress. To our knowledge, there has been no study focusing on oxidative metabolism specifically in Asperger syndrome (a milder form of autism) or comparing this metabolism with other psychiatric disorders. In this study, total antioxidant status (TAOS), non-enzymatic (glutathione and homocysteine) and enzymatic (catalase, superoxide dismutase, and glutathione peroxidase) antioxidants, and lipid peroxidation were measured in plasma or erythrocyte lysates in a group of adolescent patients with Asperger syndrome, a group of adolescents with a first episode of psychosis, and a group of healthy controls at baseline and at 8–12 weeks. TAOS was also analyzed at 1 year. TAOS was reduced in Asperger individuals compared with healthy controls and psychosis patients, after covarying by age and antipsychotic treatment. This reduced antioxidant capacity did not depend on any of the individual antioxidant variables measured. Psychosis patients had increased homocysteine levels in plasma and decreased copper and ceruloplasmin at baseline. In conclusion, Asperger patients seem to have chronic low detoxifying capacity. No impaired detoxifying capacity was found in the first-episode psychosis group in the first year of illness. [Copyright &y& Elsevier]