Thiamine pyrophosphate diminishes nitric oxide synthesis in endothelial cells.

Although thiamine pyrophosphate (TPP) is considered a protective agent for endothelial cells, it is still unknown if this is associated with nitric oxide (NO) synthesis. Our aim was to evaluate the synthesis of NO in endothelial cells incubated with TPP and high glucose concentrations. Endothelial cells from the umbilical cord vein from newborns (n = 20), were incubated with 5, 15 or 30 mmol/L glucose, in absence or presence of 0.

Increase in nitric oxide levels and mitochondrial membrane potential in platelets of untreated patients with major depression.

Alterations in platelet activity have been associated with the onset of major depressive disorder (MDD) and with ischemic cardiovascular events through mechanisms that remain unknown. The present study evaluated nitric oxide (NO) levels, mitochondrial membrane potential (PMMP), and P-selectin expression in platelets from 30 untreated MDD patients and 30 matched controls by flow cytometry. In addition, tryptophan and serotonin concentrations were measured in the whole blood by high performance liquid chromatography.

Could thiamine pyrophosphate be a regulator of the nitric oxide synthesis in the endothelial cell of diabetic patients?

Thiamine (Vitamin B1) is considered an essential micronutrient for humans; its deficient intake brings about the Wernicke-Korsakoff syndrome (encephalopathy and psychosis) or beriberi (a neurological and cardiovascular disease). Once thiamine enters the cells it is phosphorylated by thiamine pyrophosphokinase (TPPK), and converted into the coenzyme thiamine pyrophosphate (TPP), the active form of thiamine. TPP is a relevant cofactor for transketolase (TK), α-ketoglutarate dehydrogenase (αKDH), and pyruvate dehydrogenase (PDH), all these enzymes are fundamental for glucose metabolism.

Incubation with DNase I inhibits tumor cell proliferation.

Background: Deoxyribonuclease I (DNase-I) plays an important role in the elimination of damaged-, aging- or cancer cells. Various authors suggest that programmed cell death (PCD) is attenuated in cancer cells due to a reduced activity of DNase-I.

Material And Methods: In this work, we evaluated cell viability (violet crystal stain), cell proliferation (tritiated thymidine) and DNA degradation of tumoral cells (Calu-1, SK-MES-1, HeLa, HEp-2, L-929) incubated with different concentrations of DNase I.

Reduced NO synthesis and eNOS mRNA expression in endothelial cells from newborns with a strong family history of type 2 diabetes.

Background: A deficient synthesis of nitric oxide (NO) may play a role in the early endothelial dysfunction of healthy humans with a strong family history of type 2 diabetes (DM2). In this study, we evaluate the intracellular synthesis of NO and the expression of eNOS transcripts in human umbilical vein endothelial cells (HUVECs), exposed to high glucose concentrations, of healthy newborns with (experimental) and without (control) a strong family history of DM2.

Methods: HUVECs were incubated in M-199 culture media (containing a 5 mmol/L physiological glucose concentration) or supraphysiological glucose concentrations (15 or 30 mmol/L), for 48 h.

HUVECs from newborns with a strong family history of diabetes show diminished ROS synthesis in the presence of high glucose concentrations.

Background: A family history of type 2 diabetes mellitus (DM) increases the probability to develop DM and endothelial dysfunction. The probable mechanism involves augmented reactive oxygen species (ROS) synthesis. The aim of this study was to evaluate the synthesis of ROS in human umbilical vein endothelial cells (HUVECs) obtained from healthy newborns with (experimental) and without (control) a strong family history of type 2 DM, exposed to different glucose concentrations.

A fungal tRNA of Aspergillus niger induces IFN-beta synthesis in HEp-2 cells.

In this work, we evaluated the capacity of a fungal transfer RNA (F-tRNA) from Aspergillus niger to protect HEp-2 cells against a viral infection, and as an inducer of IFN-beta synthesis. HEp-2 cells previously incubated with F-tRNA, polyI:polyC, or IFN-alpha, at different concentrations for 24 h were infected with 200 pfu of adenovirus type 6 (AdV-6); after 5 days, we determined cellular viability, cytopathic effect of the virus, optimal concentration necessary to inhibit the cytopathic effect, and IFN-beta expression by RT-PCR. Results showed that HEp-2 cells treated with F-tRNA were less susceptible to the cytopathic effect of AdV-6 infection than those incubated with polyI:polyC (p < 0.