As the altitude increases, the partial pressure of oxygen will decrease and cause hypobaric hypoxia conditions. During hypoxia, the anaerobic glycolysis will be activated, which is facilitated by the lactate dehydrogenase (LDH) enzyme. This study aimed to analyze the LDH-specific activity in rat muscle and liver tissue, as well as lactate and glucose levels in blood plasma after intermittent hypobaric hypoxia exposure. Twenty-five Wistar rats were divided into five groups: one control group and four hypobaric hypoxia (HH) exposure groups consisting of group 1 (1× HH), group 2 (2× HH), group 3 (3× HH), and group 4 (4× HH) with a range of 7 days between exposure. This study found that LDH-specific activity increased in muscle tissues in group 1, but then decreased in the intermittent group (groups 2–4). The change in LDH-specific activity in muscle tissues was similar to the change in lactate plasma levels. Interestingly, in liver tissues, there was a slight increase in the LDH-specific activity in group 1, and it started to increase significantly in group 2 and kept increasing in groups 3 and 4. The change in LDH-specific activity in liver tissues was similar to the change in glucose plasma level. We conclude that the LDH activity in muscle tissue contributes to lactate plasma levels, but the LDH activity in liver tissue contributes to maintaining glucose plasma after intermittent hypobaric hypoxia exposures. This finding could be implemented in individuals who experience intermittent hypoxia exposures or in various diseases with hypoxic conditions as their pathogenesis

In a hypoxic state, fatty acid breakdown reaction may be inhibited due to a lack of oxygen. It is likely that the fatty acids will be stored as triacylglycerol. The aim of this study was to analyse triacylglycerol synthesis in the liver after intermittent hypobaric hypoxia (HH) exposures. Samples are liver tissues from 25 male Wistar rats were divided into 5 groups: control group (normoxia), group I (once HH exposure), group II (twice HH exposures), group III (three-times HH exposures) and group IV (four-times HH exposures). The triacylglycerol level, mRNA expression of HIF-1α and PPAR-γ were measured in rat liver from each group. We demonstrated that triacylglycerol level, mRNA expression of HIF-1α and PPAR-γ is elevated in group I significantly compared to control group. In the intermittent HH groups (group II, III and IV), mRNA expression of HIF-1α and PPAR-γ tends to downregulate near to control group. However, the triacylglycerol level is still found increased in the intermittent HH exposures groups. Significant increasing of triacylglycerol level was found especially in group IV compared to control group. We conclude that intermittent HH exposures will increase the triacylglycerol level in rat liver, supported by the increasing of HIF-1α and PPAR-γ mRNA expression that act as transcription factor to promote triacylglycerol synthesis.

Expression of manganese superoxide dismutase in rat blood, heart and brain during induced systemic hypoxia

Background: Preeclampsia is one of the factors causing the high maternal mortality rate. The risk of morbidity and mortality is higher in Early Onset Preeclampsia (EOPE). Failure of spiral artery remodeling can cause oxidative stress that can inhibit placental development and increase trophoblast apoptosis. Objective: This study aims to analyze the oxidative stress and apoptosis of EOPE placentas. Methods: This study is an observational study with a cross-sectional design. A total of 31 EOPE placentas and 31 normal term placentas were used to measure the concentration of malondialdehyde (MDA) and the relative mRNA expression of FOXO3 and CASP3 using the spectrophotometric and RT-qPCR methods. Results: There was no difference in MDA concentration (p = 0.580) and FOXO3 (p = 0.467) and CASP3 (p = 0.243) mRNA expression in the normal and EOPE groups. There was a strong positive correlation between FOXO3 and CASP3 mRNA expression in the normal (p= 0.0001; r = 0.938) and EOPE groups (p = 0.0001; r = 0.855). There was no correlation between MDA concentration to FOXO3 (p = 0.124; r = 0.282) and CASP3 (p = 0.569; r = 0.106) mRNA expression in normal placenta. There was positive correlation between MDA concentration to FOXO3 (p = 0.016; r = 0.429) and CASP3 mRNA expression in EOPE placenta (p = 0.028; r = 0.395). Conclusion: These results indicate that cell integrity is still maintained through the autophagy process and the level of apoptosis in the EOPE placenta is regulated by ROS through FOXO3.

Objective: The aim of this study was to analyze the effect of avidin treatment on cell viability, proliferation and cyclin D1 expression in colorectal cancer cells HT-29. Methods: Colorectal cancer cell line HT-29 incubated with 50, 100, 150, and 200 μg/mL of avidin concentration during 24, 48, and 72 hours, then the cell viability and proliferation were analyzed. Each avidin concentration was conducted together with HT-29 cell line without avidin treatment as a control group. The cell viability was measured by MTS assay and the proliferation was measured by BrdU (5-bromo-2′-deoxyuridine) cell proliferation assay. According to cell viability and proliferation result, we determined the 100 μg/mL avidin concentration for analyzing mRNA and protein of cyclin D1. Results: We demonstrated that the viability and proliferation of HT-29 cells were significantly decreased in all concentration of avidin treatment compared to control. The cell proliferation showed larger reduction in avidin treatment rather than cell viability. This proves avidin could inhibit proliferation of colorectal cancer cell HT-29 quite well. The expression of cyclin D1, both mRNA and protein, was also significantly decreased after the avidin treatment group compared to control group, it supports the suppression of proliferation result. Conclusion: We concluded that avidin treatment could decrease cell viability and proliferation, accompanied by suppression of cyclin D1 expression in colorectal cells HT-29.