An investigation was conducted to study the changes in body weight and blood lipids during Ramadan fasting in men on hypocaloric diets. Sixteen healthy male college students were fed a high-carbohydrate diet for the first 2 wk (means 1696 kcal/d), followed by another 2 wk of high-fat diet (means 1834 kcal/d). Fasting blood samples were taken on days 0 (base line), 14, and 28 and were analyzed for triglycerides (TGs) and cholesterol. By the end of Ramadan, body weight, blood TGs, and high-density lipoprotein cholesterol (HDL-chol) had decreased significantly (p less than 0.05), low-density lipoprotein cholesterol (LDL-chol) had increased, and total cholesterol had not changed compared with base-line values. The variance in blood lipid levels was explained by weight change through linear and curvilinear regression models. The findings contribute to a better understanding of the contrasting results reported by various investigators and they may be useful in regulating blood lipid levels through Ramadan fasting.

In Islamic fasting, participants abstain from food and water between dawn and sunset. This study was conducted to determine the changes in blood urea and glucose and their associations with energy-containing nutrients in men during the Islamic fasting month of Ramadan. Sixteen healthy male college students consumed a high-carbohydrate diet for 2 wk followed by a high-fat diet for the next 2 wk. Fasting blood samples were taken on day 0 (base line), 14, and 28, and analyzed for urea and glucose. At the end of the fasting period the blood urea level increased significantly (p less than 0.05) and the glucose level decreased. At day 14, blood urea was negatively correlated to sucrose intake (p less than 0.01) and at day 28, the relationship between blood glucose and energy intake was negative (p less than 0.02). The findings suggest possible use of a Ramadan fasting model for studies related to energy metabolism and regulation of energy intake.

Mimosine, a non-protein amino acid, is mainly known for its action as a reversible inhibitor of DNA replication and, therefore, has been widely used as a cell cycle synchronizing agent. Recently, it has been shown that mimosine also induces apoptosis, as mainly reflected in its ability to elicit characteristic nuclear changes. The present study elucidates the mechanism underlying mimosine's apoptotic effects, using the U-937 leukemia cell line. We now demonstrate that in isolated rat liver mitochondria, mimosine induces mitochondrial swelling that can be inhibited by cyclosporine A, indicative of permeability transition (PT) mega-channel opening. Mimosine-induced apoptosis was accompanied by formation of hydrogen peroxide and a decrease in reduced glutathione levels. The apoptotic process was partially inhibited by cyclosporine A and substantially blocked by the antioxidant N-acetylcysteine, suggesting an essential role for reactive oxygen species formation during the apoptotic processes. The apoptosis induced by mimosine was also accompanied by a decrease in mitochondrial membrane potential, cytochrome c release and caspase 3 and 9 activation. Our results thus imply that mimosine activates apoptosis through mitochondrial activation and formation of H2O2, both of which play functional roles in the induction of cell death.

Summary Naphthoquinones, such as menadione, display lower toxicity than anthracyclins used in cancer chemotherapy. Novel anti‐leukaemic compounds comprised of chloro‐amino‐phenyl naphthoquinones with substitutions on the benzoic ring were developed. Structure–activity relationship studies indicated that the analogue with both methyl and amine substitutions (named TW‐92) was the most efficient in killing leukaemic cells. Treatment of U‐937 promonocytic cells with TW‐92 induced apoptotic or necrotic cell death, dependent on incubation and dose conditions. TW‐92 induced rapid phosphorylation of p38 mitogen‐activated protein kinase (p38MAPK) and of extracellular signal‐regulated protein kinases (ERK1/2). The generation of apoptosis was preceded by intracellular H2O2 accumulation accompanied by glutathione depletion, the former inhibited by di‐phenyl‐iodonium (DPI), an inhibitor of NADPH oxidase. TW‐92 induced swelling of isolated rat liver mitochondria, indicative of a direct effect on mitochondria. Apoptosis in intact cells was accompanied by a decrease in mitochondrial membrane potential, cytochrome c release and caspase activation. In addition, the level of Mcl‐1, an anti‐apoptotic regulatory protein, was down‐regulated, whereas the expression of the pro‐apoptotic BAX was elevated. Finally, TW‐92 exerted strong pro‐apoptotic and necrotic effects in primary acute myeloid leukaemia samples when given in submicromolar concentrations. Together, these findings demonstrate that TW‐92 may provide an effective anti‐leukaemic strategy.

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