Hepatoprotective and antidiabetic effects of apple cider vinegar [A prophetic medicine remedy] on the liver of male rats

Background: Diabetes mellitus is associated with biochemical and pathological alterations in the liver. The aim of this study was to investigate the effects of apple cider vinegar [ACV] on serum biochemical markers and histopathological changes in the liver of diabetic rats for 30 days. Effects were evaluated using streptozotocin [STZ]-induced diabetic rats as an experimental model

Materials and Methods: Diabetes mellitus was induced by a single dose of STZ [65 mg/kg] given intraperitoneally. Thirty wistar rats were divided into three groups: control group, STZ-treated group and STZ plus ACV treated group [2 ml/kg BW]. Animals were sacrificed 30 days post treatment

Results: Biochemical results indicated that, ACV caused a significant decrease in glucose, TC, LDL-c and a significant increase in HDL-c. Histopathological examination of the liver sections of diabetic rats showed fatty changes in the cytoplasm of the hepatocytes in the form of accumulation of lipid droplets, lymphocytic infiltration. Electron microscopic studies revealed aggregations of polymorphic mitochondria with apparent loss of their cristae and condensed matrices. Besides, the rough endoplasmic reticulum was proliferating and fragmented into smaller stacks. The cytoplasm of the hepatocytes exhibited vacuolations and displayed a large number of lipid droplets of different sizes. On the other hand, the liver sections of diabetic rats treated with ACV showed minimal toxic effects due to streptozotocin. These ultrastructural results revealed that treatment of diabetic rats with ACV led to apparent recovery of the injured hepatocytes. In prophetic medicine, Prophet Muhammad peace is upon him strongly recommended eating vinegar in the Prophetic Hadeeth: "vinegar is the best edible"

Conclusion: This study showed that ACV, in early stages of diabetes induction- can decrease the destructive progress of diabetes and cause hepatoprotection against the metabolic damages resulting from streptozotocin- induced diabetes mellitus

Safety and outcome of treatment of metastatic melanoma using 3-bromopyruvate: a concise literature review and case study / 癌症

3-Bromopyruvate (3BP) is a new, promising anticancer alkylating agent with several notable functions. In addition to inhibiting key glycolysis enzymes including hexokinase II and lactate dehydrogenase (LDH), 3BP also selectively inhibits mitochondrial oxidative phosphorylation, angiogenesis, and energy production in cancer cells. Moreover, 3BP induces hydrogen peroxide generation in cancer cells (oxidative stress effect) and competes with the LDH substrates pyruvate and lactate. There is only one published human clinical study showing that 3BP was effective in treating fibrolamellar hepatocellular carcinoma. LDH is a good measure for tumor evaluation and predicts the outcome of treatment better than the presence of a residual tumor mass. According to the Warburg effect, LDH is responsible for lactate synthesis, which facilitates cancer cell survival, progression, aggressiveness, metastasis, and angiogenesis. Lactate produced through LDH activity fuels aerobic cell populations inside tumors via metabolic symbiosis. In melanoma, the most deadly skin cancer, 3BP induced necrotic cell death in sensitive cells, whereas high glutathione (GSH) content made other melanoma cells resistant to 3BP. Concurrent use of a GSH depletor with 3BP killed resistant melanoma cells. Survival of melanoma patients was inversely associated with high serum LDH levels, which was reported to be highly predictive of melanoma treatment in randomized clinical trials. Here, we report a 28-year-old man presented with stage IV metastatic melanoma affecting the back, left pleura, and lung. The disease caused total destruction of the left lung and a high serum LDH level (4,283 U/L). After ethics committee approval and written patient consent, the patient received 3BP intravenous infusions (1-2.2 mg/kg), but the anticancer effect was minimal as indicated by a high serum LDH level. This may have been due to high tumor GSH content. On combining oral paracetamol, which depletes tumor GSH, with 3BP treatment, serum LDH level dropped maximally. Although a slow intravenous infusion of 3BP appeared to have minimal cytotoxicity, its anticancer efficacy via this delivery method was low. This was possibly due to high tumor GSH content, which was increased after concurrent use of the GSH depletor paracetamol. If the anticancer effectiveness of 3BP is less than expected, the combination with paracetamol may be needed to sensitize cancer cells to 3BP-induced effects.