Whether overexpressed connexin26 in pancreatic cancer is a cause of impaired glucose tolerance remains to be elucidated in further experimental studies.

No abstract

In vitro lipid peroxidation of brain cell membranes was recorded directly by monitoring the concomitant photon emission. Chemiluminescence appeared spontaneously after disintegration of vital brain cells (pig brain cell homogenate, isolated oligodendrocytes), decreasing the high intracellular ascorbate concentration in the vital glial cell (1 mmol/L) to a lower overall concentration (<100 µmol/L). This had a prooxidant effect in the homogenate. Intracellular high antioxidant ascorbate concentrations were also efficient at protecting membrane lipids of vital oligodendrocytes against extracellular low prooxidant ascorbate concentrations (50 µmol/L). The intramembranous α‐tocopherol content limited the antioxidant efficiency of ascorbate. With physiological concentrations (0.4 nmol of iron to 0.1 nmol of tocopherol per milliliter of membrane suspension), a 50% inhibition of lipid peroxidation was obtained with 410 nmol/ml ascorbate; this was reduced to 90 nmol/ml in the case of fivefold increased tocopherol content. So in vivo ascorbate concentrations were sufficient to protect against lipid peroxidation. Only when endogenous tocopherol was decreased to 20% was the in vivo intracellular ascorbate concentration too small for antioxidative protection of lipids. The product of tocopherol concentration and ascorbate concentration, effective for 50% inhibition of lipid peroxidation, remained constant. When iron concentrations were increased 104‐fold, maximal chemiluminescence and malondialdehyde formation were increased twofold and less than 50%, respectively. This quantitative description of the interactions between vitamin E, vitamin C, and iron are relevant to the modification of interpretations of pathological conditions in parkinsonian brains. The chemiluminescent indicator reaction was characterized as a separate step following lipid peroxidation and malondialdehyde formation. Its relevance as a new tool for sensitive monitoring of changing cell vitality, e.g., by virus infection of cells or by endogenous metabolites, is discussed.