Intracellular Na+ is approximately two times higher in diabetic cardiomyocytes than in control. We hypothesized that the increase in Na+1 activates the mitochondrial membrane Na+/Ca2+ exchanger, which leads to loss of intramitochondrial Ca2+, with a subsequent alteration (generally depression) in bioenergetic function. To further evaluate this hypothesis, mitochondria were isolated from hearts of control and streptozotocin-induced (4 weeks) diabetic rats. Respiratory function and ATP synthesis were studied using routine polarography and 31P-NMR methods, respectively. While addition of Na+ (1–10 mM) decreased State 3 respiration and rate of oxidative phosphorylation in both diabetic and control mitochondria, the decreases were significantly greater for diabetic than for control. The Na+ effect was reversed by providing different levels of extramitochondrial Ca2+ (larger Ca2+ levels were needed to reverse the Na+ depressant effect in diabetes mellitus than in control) and by inhibiting the Na+/Ca2+exchanger function with diltiazem (a specific blocker of Na+/Ca2+ exchange that prevents Ca2+ from leaving the mitochondrial matrix). On the other hand, the Na+ depressant effect was enhanced by Ruthenium Red (RR, a blocker of mitochondrial Ca2+ uptake, which decreases intramitochondrial Ca2+). The RR effect on Na+ depression of mitochondrial bioenergetic function was larger in diabetic than control. These findings suggest that intramitochondrial Ca2+ levels could be lower in diabetic than control and that the Na+ depressant effect has some relation to lowered intramitochondrial Ca2+. Conjoint experiments with 31P-NMR in isolated superfused mitochondria embedded in agarose beads showed that Na+ (3–30 mM) led to significantly decreased ATP levels in diabetic rats, but produced smaller changes in control. These data support our hypothesis that in diabetic cardiomyocytes, increased Na+ leads to abnormalities of oxidative processes and subsequent decrease in ATP levels, and that these changes are related to Na+ induced depletion of intramitochondrial Ca2+.

Lactobacilli are  widely used  in clinical  practice as probiotics, biologically  active  additives  and probiotic products for functional nutrition. Some  probiotics can  be considered as bacterial vaccines  due  to induction of immune response, accompanied by production of specific antibodies. The aim of the present study was to evaluate  the state of cellular and humoral immunity in women  by using probiotic strains of lactobacilli. The  study  included 31 healthy  women  aged  25-45  years.  As a source  of probiotic lactobacterial complex, we used  the  “Provag” preparation (RU  77.99.11.003.E.003746.02.11 of 11.02.2011, 1 capsule  contains 109 Lactobacillus  gasseri 57C,  Lactobacillus  fermentum  57A и Lactobacillus  plantarum  57B).  The  drug  was used for 30 days, at a rate  of one  capsule  per day. The  immune system was examined twice: before  administering the drug and after 30 days of treatment. The study of blood  lymphocyte populations and subpopulations was performed by flow cytometry using direct immunofluorescence technique. The concentration of IgA, IgM, IgG in blood serum was determined using enzyme  immunoassay. To determine specific antibodies, we used passive hemagglutination reaction with erythrocyte diagnosticum. The complex of probiotic lactobacilli Lactobacillus gasseri, Lactobacillus  fermentum  and  Lactobacillus  plantarum corresponding to the “Provag” preparation was used as a source  of antigen. It has been revealed  that  the number of T and B lymphocytes in peripheral blood increased after  30 days  of treatment with  the  probiotic preparation “Provag” in  healthy  women. Elevated contents of T cells was due to the T helper  cell fraction. Increased levels of T helpers and B lymphocytes were associated with stimulation of humoral immunity, as evidenced by increasing concentration of IgA and  IgG in blood  serum.  By means  of passive hemagglutination reaction, we have found  that  90% of healthy  women showed increased concentrations of specific IgA in blood after 30 days of treatment with “Provag” preparation.

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