Toxoplasmosis is a common parasitic infection in the world. Since increased free radicals and oxidative stress are reported in many parasitic diseases the purpose of the present study was to evaluate the oxidative stress in acute and chronic toxoplasmosis. RH strains of Toxoplasma tachyzoites were used in the present study. Twenty‐five female rats were infected with the parasite while 25 other rats were as the control group that received normal saline. Zero‐, 5‐, 7‐, 10‐, and 45‐day postinfection (DPI) blood samples were taken. Some parameters related to oxidant and antioxidants such as antioxidant enzymes, malondialdehyde, and total antioxidant capacity were measured. On day 7 after infection, GPX activity and GSH level were significantly increased and in the mentioned day the amount of total antioxidant capacity was significantly reduced. In other cases, there were no significant differences between the groups in different days. Overall, based on the results it seems that, on day 7 after infection, in infected rats responses to oxidative stress were triggered and led to decrease of total antioxidant capacity. Furthermore, glutathione was increased to cope with stress. It seems that probably antioxidant defense system entered the infection to the chronic phase and changed the parasites stage.

Aerobic glycolysis rate is higher in breast cancer tissues than adjacent normal tissues which providethe ATP, lactate and anabolic precursors required for tumourgenesis and metastasis. Lactate dehydrogenase (LDH) is a critical enzyme during aerobic glycolysis as it is typically responsible for the production of lactate and regeneration of NAD+, which allows for the continued functioning of glycolysis even in the absence of oxygen. LDH has been found to be highly expressed in breast tumors. Enzyme kinetic characteristics is related to environmentinvolving the enzyme, and tumor microenvironment has distinct features relative to adjacent normal tissues, thus we hypothesized that LDH should have different kinetic characteristics in breast tumors compared to normal breast tissues. LDH was partially purifiedfrom human breast tumors and normal tissues, which were obtained directly from operating room. TheMichaelis-Menten constant (Km), maximum velocity (Vmax), activation energy (Ea) and enzyme efficiency in breast tumors and normal tissueswere determined. It was found that tumor LDH affinity in forward reaction was the same as normal LDH but Vmax of cancerous LDH was higher relative to normal LDH. In reverse reaction, affinity of tumor LDH for lactate and NAD+ was lower than normal LDH, also enzyme efficiency for lactate and NAD+ was higher in normal samples. The Ea of reverse reaction was higher in cancerous tissues. It was concluded that thelow LDH affinity for lactate and NAD+ is a valuable tool for preserving lactate by cancer cells. We also conclude that increasing of LDH affinity may be a valid molecular target to abolish lactate dependent tumor growth and kinetic characteristics of LDH could be a novel diagnostic parameter for human breast cancer.

Objective: Okra (Abelmoschus esculentus) is a tropical vegetable that is rich in carbohydrates, fibers, proteins and natural antioxidants. The aim of the present study was to evaluate the effects of Okra powder on pancreatic islets and its action on the expression of PPAR-gamma and PPAR-alpha genes in pancreas of high-fat diet (HFD) and streptozotocin-induced diabetic rats. Materials and Methods: In this experimental study, diabetes was induced by feeding HFD (60% fat) for 30 days followed by an injection of streptozotocin (STZ, 35 mg/kg). Okra powder (200 mg/kg) was given orally for 30 days after diabetes induction. At the end of the experiment, pancreas tissues were removed and stained by haematoxylin and Eozine and aldehyde fuchsin for determination of the number of beta-cells in pancreatic islets. Fasting blood sugar (FBS), Triglycerides (TG), cholesterol, high density lipoprotein (HDL), low density lipoprotein (LDL), and insulin levels were measured in serum. Moreover, PPAR-gamma and PPAR-alpha mRNAs expression were measured in pancreas using real time polymerase chain reaction (PCR) analysis. Results: Okra supplementation significantly decreased the elevated levels of FBS, total cholesterol, and TG and attenuated homeostasis model assessment of basal insulin resistance (HOMA-IR) index in diabetic rats. The expression levels of PPAR-gamma and PPAR-alpha genes that were elevated in diabetic rats, attenuated in okra-treated rats (P < 0.05). Furthermore, okra improved the histological damages of pancreas including vacuolization and decreased beta-cells mass, in diabetic rats. Conclusion: Our findings confirmed the potential anti-hyperglycemic and hypolipidemic effects of Okra. These changes were associated with reduced pancreatic tissue damage. Down-regulation of PPARs genes in the pancreas of diabetic rats after treatment with okra, demonstrates that okra may improve glucose homeostasis and beta-cells impairment in diabetes through a PPAR-dependent mechanism.

High aerobic glycolysis, as one of the hallmarks of cancer cells, requires nicotinamide adenine dinucleotide (NAD+) as a vital co‑factor, to guarantee the flow of glycolysis. Malate dehydrogenase (MDH), as an important enzyme in cancer metabolism, is a source of NAD+ additional to lactate dehydrogenase (LDH). The current study aimed to elucidate the kinetic parameters of MDH in human breast cancer and evaluate its supportive role in the glycolysis pathway. The Michaelis‑Menten constant (Km) and maximum velocity (Vmax) of MDH were determined in the crude extracts of human breast tumors and healthy tissue samples, which were obtained directly from the operating theatre. To assess the potential role of MDH in supporting glycolysis, the MDH activity was measured when the LDH activity was inhibited by different concentrations of oxamate, an inhibitor of LDH in breast cancer cell lines. The Km of cancerous MDH (C‑MDH) was the same as the healthy MDH, although the Vmax of C‑MDH was higher relative to the healthy MDH. Notably, the MDH activity was increased in the MDA‑MB‑231 cell line, which was treated with the LDH inhibitor (oxamate), but not in the MCF‑7 cell line (P<0.05). The higher tendency of C‑MDH for NAD+ and malate generation in cancer cells is an effective approach for supporting glycolysis. Increasing MDH activity in the absence of LDH demonstrates the supportive role of MDH in glycolysis. Therefore, decreasing MDH activity and expression in a forward reaction may present as a valid molecular target to abolish its potential effect on tumor metabolism.