In this study, effects of vitaminB12 on embryonic development have been investigated by supplying vitaminB12 on a hypoxia-induced embryo culture. 9.5-day-old embryos from Wistar albino adult pregnant rats were used in our experimental set up.10 μM and 100 μM vitaminB12 were added to culture medium which is then exposed to in vitro hypoxia. Additionally, 11.5-day-old embryos and yolksacs were examined morphologically. Different vitaminB12 doses are compared within experimental groups. It was found that both control and experimental groups in 11.5-day-old embryos are at same developmental stage. It was also determined that oxygen deficiency influenced embryonic development and yolk sac vascularity in hypoxia group, are lagging behind in all experimental groups (P < 0.05). However, the development of vitaminB12 embryos were similar to control group under normoxic conditions (P > 0.05). It was also observed that development was compensated through supplement of vitaminB12 to hypoxia group (P < 0.05). It was indicated that the development in H + 100 μM vitB12 groups was quite close to control group. However, development of H + 10 μM vitB12 embryos were in parallel with hypoxic group. Furthermore, H + 100 μM vitB12 group showed higher embryonic development than H + 10 μM vitB12 group (P < 0.05).VitaminB12 treatment has been used to prevent intrauterine growth restriction which can be caused by many different pharmacological agents. However, nobody has investigated effects of vitaminB12 on hypoxia-induced early embryo growth retardation. In the light of our findings, administration of 100 μM vitaminB12 restores damage of embryonic development due to hypoxia and this application also increases embryonic vascularity and circulation. Thus, supplementation of vitaminB12 can be offered as a therapeutic approach towards cell death and diseases such as neurovascular and cardiovascular diseases and in the near future.

Objectives: The Pasteur effect in cellular energy metabolism is defined as the switch to anaerobic glycolysis due to alterations in ambient oxygen concentration or inhibition of the electron transport chain (ETC) and oxidative phosphorylation. This study aimed to determine the effect of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection on the energy metabolism of leukocytes among Coronavirus Disease 2019 (COVID-19) patients at various stages. Methods: A total of 90 cases were analyzed in asymptomatic, mild, moderate, and severe COVID-19 patients. Levels of aerobic glycolysis intermediates and products of anaerobic glycolysis were measured in leukocytes with liquid chromatography-tandem mass spectrometry (LC-MS/MS) analysis. Results: A decrease in the rate of aerobic glycolysis was found as the disease progressed (p-values<0.001), while the anaerobic glycolysis rate was unchanged in all study groups because lactate levels had no difference between asymptomatic, mild, moderate, and severe groups (p=0.754). Moreover, the ratios of lactate to Tricarboxylic Acid (TCA) cycle parameters demonstrated a significant reduction in the rate of aerobic glycolysis of COVID-19 patients at different stages (p-values<0.001). Furthermore, Receiver Operating Characteristic (ROC) curve analysis for citrate, alpha-ketoglutarate, fumarate, lactate, lactate/citrate, lactate/alpha-ketoglutarate, and lactate/fumarate had significant cut-off values in Moderate and Severe patients (p<0.001). Conclusions: Our results suggest that the Pasteur effect from aerobic to anaerobic glycolysis was shown to be induced as the severity of COVID-19 progresses.