Negative effect of feeding with high energy diets on testes and metabolic blood parameters of male Japanese quails, and positive role of milk thistle seed.

In this study, it was aimed to investigate the changes in testicular tissue and cell count, testicular oxidative stress and some metabolic blood parameters of male broiler Japanese quails fed with high energy diet and milk thistle (Silybum marianum) seed. One hundred-twenty male 15-day-old Japanese quail chicks were divided into 4 equal groups with 30 each. The applications in each group were repeated 3 times with 10 animals each. Control group was fed with basal diet. Milk thistle seed group was fed with diet including 1% milk thistle seed. High energy diet group was fed with high energy diet including 10% corn syrup. High energy diet + milk thistle seed group was fed with high energy diet including 10% corn syrup along with 1% milk thistle seed. The feeding period in all groups was 35 days. When the quails reached 50 days old, a total of 48, 12 from each group (4 from each replication) were euthanized and blood samples and testes were collected. Compared with the control group, significant increases in body weight, serum cholesterol and glucose level, aspartate aminotransferase activity and testicular malondialdehyde level; however, significant decreases in serum testosterone level, testicular glutathione peroxidase activity, counts of round and elongated spermatid and sperm as well as histopathologically, significant decreases in seminiferous tubular diameter and seminiferous epithelium thickness, and marked disorganization in germinal cells were determined in quails fed with high energy diet. It was observed that almost all of the disturbances in testicular tissue, cell number, oxidant-antioxidant balance and metabolic blood parameters caused by feeding with high energy diet were significantly prevented by supplementation of milk thistle seed to the diet with high energy. On the other hand, alone milk thistle seed and high energy diet + milk thistle seed administrations decreased body weight in comparison to control and high energy diet groups. As a result, feeding with high energy diet causes disturbances in testes of male quails by affecting liver metabolic functions and testicular oxidant-antioxidant balance, but milk thistle seed addition to diet plays a protective role.

Essential oil composition, antioxidant and antifungal activities of Salvia sclarea L. from Munzur Valley in Tunceli, Turkey.

The essential oil composition and in vitro antioxidant and antifungal activity of the Salvia sclarea L. from Munzur Valley in Tunceli, Turkey were evaluated in this research. The in vitro antifungal activity of ethanol, hexane and aqueous extracts of S. sclarea against pathogen fungi Epicoccum nigrum and Colletotrichum coccodes were investigated. The essential oil of aerial parts of S. sclarea was obtained by hydrodistillation and was analysed by GC and GC­MS. Total antioxidant status was determined by using Rel assay diagnostics TAS assay kit (Lot.RL024) by Multiscan FC (Thermo). 33 compounds were identified representing the 85.0% of the total oil. The most abundant components (>5%) of the S. sclarea essential oils were caryophyllene oxide (24.1%), sclareol (11.5%), spathulenol (11.4%), 1H-naphtho (2,1,6) pyran (8.6%) and b­caryophyllene (5.1%). The best antifungal and antioxidant effect was seen in ethanolic S. sclarea extract. It can be said that Salvia sclerae could be used as natural antioxidant.

Bistability analysis of an apoptosis model in the presence of nitric oxide.

Bistability in apoptosis, or programmed cell death, is crucial for the healthy functioning of multicellular organisms. The aim in this study is to show the presence of bistability in a mitochondria-dependent apoptosis model under nitric oxide effects using chemical reaction network theory. The model equations are a set of coupled ordinary differential equations arising from the assumed mass action kinetics. Whether these equations have a capacity for bistability (cell survival and apoptosis) is determined using a modular approach in which the model is decomposed into modules. Each module contains only a subset of the whole model and is analyzed separately. It is seen that bistability in a module is preserved throughout the whole model after adding the remaining reactions in the pathway on these modules. It is also found that inhibitor effect of some proteins and the appearance of a reacting protein in a later stage as a product is a desired feature but not sufficient for bistability (in the absence of cooperativity effects). On the whole model, two apoptotic and two cell survival states are obtained depending on the initial cell conditions. The results suggest that the antiapoptotic effects of nitric oxide species are responsible for the bistable character of the apoptotic pathway when cooperativity is not assumed in the apoptosome formation.

Bistability in apoptosis: roles of bax, bcl-2, and mitochondrial permeability transition pores.

We propose a mathematical model for mitochondria-dependent apoptosis, in which kinetic cooperativity in formation of the apoptosome is a key element ensuring bistability. We examine the role of Bax and Bcl-2 synthesis and degradation rates, as well as the number of mitochondrial permeability transition pores (MPTPs), on the cell response to apoptotic stimuli. Our analysis suggests that cooperative apoptosome formation is a mechanism for inducing bistability, much more robust than that induced by other mechanisms, such as inhibition of caspase-3 by the inhibitor of apoptosis (IAP). Simulations predict a pathological state in which cells will exhibit a monostable cell survival if Bax degradation rate is above a threshold value, or if Bax expression rate is below a threshold value. Otherwise, cell death or survival occur depending on initial caspase-3 levels. We show that high expression rates of Bcl-2 can counteract the effects of Bax. Our simulations also demonstrate a monostable (pathological) apoptotic response if the number of MPTPs exceeds a threshold value. This study supports our contention, based on mathematical modeling, that cooperativity in apoptosome formation is critically important for determining the healthy responses to apoptotic stimuli, and helps define the roles of Bax, Bcl-2, and MPTP vis-à-vis apoptosome formation.