The aim of the study was to evaluate blood selenium and antioxidants as possible oxidative stress markers in Alzheimer's disease (AD) along with amyloid β42 (Aβ42) and tau by comparing them with vascular dementia (VD) and age-matched healthy controls. Selenium, total tau, Aβ42, glutathione (GSH) and malondialdehyde (MDA) levels and the activities of antioxidant enzymes were analysed in the blood of AD patients (n = 30), VD patients (n = 35) and controls (n = 40) from South India. Plasma Aβ42 level was significantly higher (P < 0.001) in both AD and VD compared to controls. Total tau and tau-to-amyloid ratio were significantly lower in both AD and VD (P < 0.001), compared to controls, and a significant difference (P < 0.01 and P < 0.05, respectively) was also observed between AD and VD. The receiver operating characteristic (ROC) curve-derived cutoff values of <3.5 for tau-to-Aβ42 ratio and <520 pg/ml for total tau showed sensitivity and specificity of around 67-72 % for differentiating AD from VD and around 90 % for AD from controls, indicating that they could serve as reliable AD-specific markers. The MDA levels were significantly higher (P < 0.001) in both dementia groups along with a significant decrease (P < 0.001) in reduced GSH levels, indicating elevated oxidative stress and altered redox status in both forms of dementia. Selenium levels did not vary significantly between the three groups. The activity of glutathione peroxidase increased in both AD and VD compared to controls, with a concomitant decrease in glutathione reductase and glucose-6-phospate dehydrogenase (P < 0.001) activity. The activity of thioredoxin reductase was significantly lower in both patient groups (P < 0.001) compared to healthy controls. No correlation was observed between selenium and activities of selenoenzymes, tau, Aβ42 or tau-to-Aβ42 ratio, when analysing independently, indicating that blood selenium may not be directly involved in Aβ production and in regulating tau/Aβ42-mediated mechanism in AD. The present study emphasizes the enhanced oxidative stress in AD pathology and plasma tau and tau-to-amyloid ratio as possible markers to differentiate AD from VD. The study also points that blood selenium may not be involved in regulating oxidative stress in AD, and a longitudinal study correlating plasma and cerebrospinal fluid (CSF) selenium and selenoprotein levels is warranted.

Many factors are involved in Alzheimer’s disease (AD) pathology including tau phosphorylation, amyloid β protein (Aβ) accumulation, lipid dysregulation, oxidative stress, and inflammation. The markers of these pathological processes in cerebral spinal fluid are used currently for AD diagnosis. However, peripheral biomarkers are the need of the hour for large population screening for AD. The main objective of the present study is to evaluate the peripheral levels of redox markers, lipid peroxidation (LPO) indicators, and pathological markers in AD patients. Blood was collected from AD patients (n = 45), controls (n = 45), and analyzed for pathological markers of AD including Aβ42 and tau, LPO, and redox indicators. Plasma Aβ42 was significantly (P < 0.001) elevated while total tau was decreased in AD compared to controls. Hydroxynonenal (HNE) and malondialdehyde (MDA) were higher (P < 0.001) in AD patients pointing the enhanced LPO in AD pathology. Receiver operating characteristic curve (ROC) analysis indicated that HNE is a better indicator of LPO compared to MDA. Plasma glutathione (GSH) level was significantly (P < 0.001) low while oxidized glutathione (GSSG) level was higher (P < 0.001) in AD patients with corresponding decrease in GSH/GSSG ratio (P < 0.001). ROC analysis indicated that GSH/GSSG ratio can be used as reliable indicator for redox imbalance in AD with a cutoff value of <8.73 (sensitivity 91.1%, specificity 97.8%). Correlation analysis revealed a positive correlation for both HNE and MDA with Aβ42 and a negative correlation with total tau. Negative correlation was observed between GSH/GSSG ratio and LPO markers. While oxidative stress has been implicated in pathology of various neurodegenerative disorders, the present study pinpoints the direct link between LPO and Aβ production in plasma of AD patients. Normally, at low amyloid concentration in body fluids, this peptide shown to function as a strong metal chelating antioxidant. However, when the Aβ production enhanced as in AD, through gain of functional transformation, Aβ evolves into prooxidant, thereby enhancing oxidative stress and LPO. Altered redox status with enhanced LPO observed in AD blood could contribute to the oxidation and S-glutathionylation proteins, which has to be addressed in future studies.

The present paper focuses on assessing the levels of various enzymatic and non-enzymatic antioxidants in selected berries of Indian sub-continent viz., gooseberry, grapes, orange and tomato. This study has revealed that orange, tomato and grapes possess predominant quantities of enzymatic antioxidants namely SOD, catalase and glutathione peroxidase respectively. The levels of antioxidants analyzed namely reduced glutathione, vitamin C and vitamin A were maximal in grapes, orange and tomato respectively. All the extracts of berries included in the present study inhibited iron induced in vitro lipid peroxidation in erythrocytes, the extend of inhibition being highest for gooseberry and orange compared to tomato and grapes which could be attributed to their in-built antioxidant system.

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Requirement, uptake, and subcellular distribution of Na2(75)SeO3 in the larvae of the insect C. cephalonica was investigated. That Se is well tolerated by C. cephalonica upto an added level of 2 ppm in the diet is suggested by the observed increase in body weight, total protein, and succinate dehydrogenase levels. Significant increases in the State 3 respiration ensued with Se supplementation up to 2 ppm in the mitochondrial oxidation of D-glycerol 1-phosphate, succinate and NADH, along with concomitant unaltered State 4 respiration, leading to enhanced RCR values. Maximal uptake of 75Se was registered in the larvae maintained on basal diet when subjected to short-term exposure to 0.5 ppm 75Se level. When exposure level was further increased up to 20 ppm, the observed decrease in the uptake of 75Se suggested that Se status of larvae itself controlled the tissue uptake. Subcellular distribution pattern revealed maximal incorporation of 75Se (cpm/g tissue) in the supernatant fraction, whereas, maximal specific 75Se activity (cpm/mg protein) was associated with the mitochondrial fraction. Autoradiography of the soluble fractions indicated the presence of single selenoprotein in the larval group with short term 2 ppm 75Se exposure. Inherent Se controls both the extent and the nature of distribution of mitochondrial 75Se incorporation. Uptake of 45Ca by the insect mitochondria was enhanced by dietary Se up to 2 ppm but was unaffected by addition of in vitro 75Se in the medium. A more fundamental role for Se in the mitochondrial energy metabolism emerges from these studies.