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In this study, the protective effects of L-arginine treatment in vivo on vascular reactivity of streptozotocin (STZ)-induced 12-week-old diabetic rats were examined. Loss of weight, polydipsia, polyphagia, hyperglycemia, hypoinsulinemia, and elevated levels of plasma cholesterol and triglyceride were observed in diabetic rats. L-arginine treatment (1 mg/mL in drinking water) did not significantly affect these metabolic and biochemical abnormalities. Plasma malondialdehyde (MDA) levels in untreated diabetic rats were also significantly higher than untreated controls. However, L-arginine treatment prevented the increase in MDA level of plasma of diabetic rats. Contractile responses, but not sensitivity to noradrenaline (NA), were significantly increased in diabetic rats compared to controls. Treatment of diabetic rats with L-arginine completely prevented the increase in NA responses. Relaxation response to acetylcholine (ACh), but not to sodium nitroprusside (SNP), in diabetic aorta has been found to be significantly decreased as compared with controls. However, there were no significant differences in pD 2 values of acetylcholine in either of the groups. L-arginine treatment increased the ACh responses to the control level. All effects of L-arginine on vascular reactivity were found to be specific for diabetic rats and not controls. These results suggest that functional abnormalities occurred in aorta from diabetic rat might at least in part result from L-arginine deficiency, and the lipid peroxidation-lowering effect of L-arginine may account for its protective effect on vascular reactivity of diabetic rats.

The effects of dietary sodium selenite and vitamin E on the microvascular permeability of rat organs such as heart, brain, kidney, liver and eye were investigated by using the Evans blue leakage method. Combined deficiency of selenium and vitamin E caused an increase in the permeability of the heart and eye with respect to their controls while it had no considerable effect on the permeability of other organs. On the other hand, toxic levels of selenium (4.2 mg/kg) in diet decreased the permeabilities in kidney, liver, and eye whereas this parameter of brain increased in the same animal group. These results suggested that low or high sodium selenite and vitamin E contents in diet could alter the microvascular permeability of different organs in different manners. It might be important to give reasonable explanations for the pathophysiology of some diseases that are characterized with organ damage and/or disfunction originated from selenium deficiency or toxicity.

interface with the antigen presenting cell. Recent evidence suggests they are actively signaling, however their role in signal initiation and propagation is still unclear. To mechanically control the agonist MCC-MHC per TCR cluster we use microcorrals of fluid supported lipid bilayer with a confined number of MCC-MHC and correspondingly bound TCR. T cell activation (measured by calcium flux) on these microcorrals is significantly reduced at low MCC-MHC concentrations, compared to cells off them. T cell activation depends not on the overall number of agonist-MHC present, but on their number per microcorral. At least two MCC-MHCs per corral are required to trigger T cell calcium flux. Cells that can cluster even more MCC-MHC per TCR cluster do not exhibit higher signaling. This result provides an extension to the heterodimer hypothesis, by which a direct complex between agonist-MHC-TCR and co-agonist-MHC-TCR is the functional signaling unit. It confirms that two MCC-MHC-TCR are required and suggests that they are sufficient for TCR nanocluster signaling.

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