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Vitamin C and Cancer
Published in Qi Chen, Margreet C.M. Vissers, Cancer and Vitamin C, 2020
Channing Paller, Tami Tamashiro, Thomas Luechtefeld, Amy Gravell, Mark Levine
While pharmacologic ascorbate appears to have cytotoxic effects on many cancer cells through hydrogen-peroxide-mediated pro-oxidant damage, in a subset of cancer cells, additional related mechanisms have been described. Cytotoxicity may be due to oxidation of ascorbate into an unstable metabolite and reversible oxidized form of ascorbate, dehydroascorbic acid [70]. Tumor cells internally reduce dehydroascorbic acid to ascorbate-triggering glutathione scavenging, inducing oxidative stress, inactivating glyceraldehyde 3-phosphate dehydrogenase, inhibiting glycolytic flux, and ultimately leading to an energy crisis leading to cell death [71,72]. For example, cultured human colorectal cancer cells with KRAS or BRAF mutations were selectively killed by pharmacologic ascorbate by depletion of intracellular glutathione. This is followed by inactivation of glyceraldehyde 3-phosphate dehydrogenase, leading to inhibition of glycolysis and death in cancer cells highly dependent on glycolysis [71]. Pharmacologic ascorbate can also induce metabolic stress by depletion of NAD in several cancer cell lines [73,74].
Oxidative Stress and the Effects of Dietary Supplements on Glycemic Control in Type 2 Diabetes
Published in Emmanuel C. Opara, Sam Dagogo-Jack, Nutrition and Diabetes, 2019
It is clear that oxidative stress is strongly associated with type 2 diabetes, as shown by various studies using different approaches, as outlined in the preceding section. The crucial question from these studies showing association between oxidative stress and type 2 diabetes is the role, if any, that oxidative stress may play in the pathogenesis of type 2 diabetes. To address this question, it is pertinent to review the metabolic pathways of glucose disposal. The primary pathway of glucose metabolism is glycolysis, through which pyruvate is generated and enters the second pathway, known as the Krebs cycle, for complete oxidation [47]. The complete oxidation of glucose to yield ATP is achieved by oxidative phosphorylation that is coupled to an electron transport chain. In the glycolytic pathway, glyceraldehyde-3-phosphate dehydrogenase enzyme catalyzes the degradation of glyceraldehyde-3-phosphate to 1,3-bisphosphoglycerate. This enzyme is a heme-containing protein that can be inhibited when oxidized severely by a burden of oxidants [48,49]. Also, the cytochrome enzymes of the electron transport chain contain the transition metal copper (Cu++), which can also be inhibited when oxidized by the abundance of ROS. The consequence of these blockages to glucose metabolism by oxidative stress would contribute to an elevation of blood glucose or hyperglycemia.
Anaerobic endurance: the speed endurance sports
Published in Nick Draper, Helen Marshall, Exercise Physiology, 2014
During the sixth step of glycolysis, catalysed by the enzyme glyceraldehyde 3-phosphate dehydrogenase, a further phosphate is bonded to the first carbon of each triose to form 1, 3-bisphosphoglycerate. In addition, two hydrogen atoms, one from G3P and one from Pi, reduce nicotinamide adenine dinucleotide (NAD+) to NADH + H+. As a co-enzyme carrier, NAD+ facilitates H atom transport for the reduction of pyruvate to form lactate, or to the mitochondria for use within aerobic metabolism. NAD+ will be described in more detail in the section on lactate below and in Chapter 12 where aerobic metabolism is discussed. In summary, step six involves the addition of a further phosphate and the removal of one hydrogen atom from each of the trioses, resulting in the formation of 1, 3-bisphos-phoglycerate, a reaction that is catalysed by glyceraldehyde 3-phosphate dehydrogenase. Up to this point, the sixth step of glycolysis, there continues to be a net loss of two ATP (net ATP = − 2).
Feasibility of olfactomedin 4 as a molecular biomarker for early diagnosis of gastric neoplasia after intestinal metaplasia
Published in Scandinavian Journal of Gastroenterology, 2023
Lixing Pang, Xin Yan, Dongxing Su, Xianbin Wu, Haixing Jiang
A quantitative real-time polymerase chain reaction (qRT-PCR) was performed to measure the mRNA expression level of OLFM4. Briefly, the total RNA was extracted from the tissues of GS, GC, and GCP using a TRIzol™ reagent. The RNA concentration and purity were detected by a spectrophotometer. The PCR amplification was conducted on cDNA synthesized from the total RNA using a reverse transcription kit. The OLFM4 primers were synthesized by Sangon Biotech (Shanghai) Co. Ltd. and sequenced as forwarding 5′-TAGGCAGCGGAGGTTCTGTGTC-3′ and reverse 5′-AATTCCAAGCGTTCCACTC TGTCC- 3′. The PCR was performed using a two-step procedure (step 1: 95 °C for 30 s [pre-denaturation]; step 2: 95 °C for 5 s and 60 °C for 34 s, 40 cycles [amplification]). Glyceraldehyde-3-phosphate dehydrogenase served as the internal control. The relative mRNA expression level of OLFM4 was calculated using the 2−ΔΔCt method.
Histological and Biochemical Changes in Adult Male Rat Liver after Spinal Cord Injury with Evaluation of the Role of Granulocyte-Colony Stimulating Factor
Published in Ultrastructural Pathology, 2020
Dalia A. Mohamed, Noura Mostafa Mohamed, Shaimaa Abdelrahaman
PCR was conducted in a final volume of 25 μl consisting of 1 μl cDNA, 1 μl of 10 pM of each primer (forward and reverse), and 12.5 μl PCR master mix (Promega Corporation, Madison, WI, USA). The volume was brought up to 25 μl using sterilized deionized water. PCR was carried out using Bio-Rad T100™ Thermal Cycle machine with a cycle sequence of 94℃ for 5 min, followed by variable cycles, each of which consists of denaturation at 94℃ for 1 min, annealing at the specific temperature corresponding to each primer of IL1B, IL 10 and TNF-α and extension at 72℃ for 1 min with an additional final extension at 72℃ for 7 min. The expression of glyceraldehyde-3-phosphate dehydrogenase (G3PDH) mRNA was examined as a reference. The expression of IL1B, IL10 and TNF-α was reported as the D cycle threshold (DCt) value (Table 1).
Chronic exposure to gamma irradiation at low-dose rates accelerates blood pressure decline associated with aging in female B6C3F1 mice
Published in International Journal of Radiation Biology, 2019
Daisaku Takai, Akiko Abe, Jun-ichiro Komura
Blood (50–70 μl) was collected from the facial vein (n = 12 per group) with a goldenrod animal lancet (MEDIpoint, Inc., Mineola, NY). An RNeasy mini kit (QIAGEN, Valencia, CA) was used to extract RNAs from the blood samples and the RT2 Profiler™ PCR Array Mouse Aging (PAMM-178Z; QIAGEN) was used to analyze the mRNA levels of the different genes associated with aging. The RT2 Profiler™ PCR Array Mouse Aging profiles the expression of 84 genes altered during aging, a major biological process and a risk factor for many diseases. The levels of glyceraldehyde-3-phosphate dehydrogenase gene were used as reference. The RT2 Profiler™ PCR Array Data Analysis version 3.5 was used to calculate the fold changes in the irradiated mice and the 95% confidence intervals of each mRNA.