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Human lymphocytes have low levels of many antioxidant enzymes however they are know to concentrate vitamin C. Cell injury, including oxidative stress effects, is associated with calcium influx so the influence of vitamin C on the maintenance of calcium levels in leukocytes was studied. Incubation of Molt-3 human lymphoblastoid cells with physiologically relevant concentrations of vitamin C and the calcium ionophore A23187 reversed the calcium influx and increased nuclear protein level associated with the ionophore alone. It is concluded that intracellular vitamin C can inhibit calcium influx into leukocytes so helping to minimise cell damage.

A wide range of DNA damage is known to be caused by reactive oxygen species (ROS). Defence against the effects of such damage include damage prevention (e.g. antioxidant activity) and the removal of damaged moieties from DNA (DNA repair). Radiation (X-ray) sensitive murine lymphoma (LY) cells were seen to be more susceptible to ROS-induced damage than were radiation resistant cells. This difference was unlikely to be due to the marginally decreased DNA excision repair capacity of the sensitive cells. Radiation sensitive cells did, however, have lower endogenous antioxidant enzyme levels. Thus, the importance of assessing all levels of a cell's response to ROS, in determining the major factors leading to increased mutagen sensitivity, is emphasised.

Aims The onset of complications in Type 2 diabetes mellitus (DM) patients cannot be predicted in individuals. Evidence suggests a link between complications and hyperglycaemia, oxidative stress and antioxidants, but causality is unclear. This study investigated baseline (entry) fasting plasma ascorbic acid, lymphocytic DNA damage and glycaemic control in Type 2 DM as part of a long-term study, the aim of which is to explore a biomarker profiling approach to identify and improve outcome in high-risk subjects. Methods A cross-sectional study, in which DNA damage, glycated haemoglobin (HbA1c), fasting plasma glucose (FPG) and ascorbic acid (AA) were measured on fasting blood samples collected from 427 Type 2 DM subjects. Results DNA damage was significantly ( P < 0.0001) and directly correlated to both FPG ( r = 0.540) and HbA1c ( r = 0.282), and was significantly ( P < 0.0001), independently and inversely correlated to plasma AA ( r = −0.449). In those subjects with both poor glycaemic control and low AA (< 48 µ m, the overall mean value for the study group), DNA damage was significantly ( P < 0.005) higher compared with those subjects with a similar degree of hyperglycaemia but with AA above the mean. Conclusions The novel finding of a significant inverse relationship between plasma AA and DNA damage in Type 2 DM indicates that poorly controlled diabetic subjects might benefit from increased dietary vitamin C. The data also have important implications for biomarker profiling to identify those subjects who might benefit most from intensive therapy. Longer-term follow-up is underway. [ABSTRACT FROM AUTHOR]