Schottky barrier height shifts depending on the interfacial layer as well as a change of the interface state charge with the forward bias while considering the presence of bulk (semiconductor) series resistance are discussed both theoretically and experimentally. It has been concluded that the barrier height shift or increase in Schottky diodes is mainly due to the potential change across the interfacial layer and the occupation of the interface states as a result of the applied forward voltage. One assumes that the barrier height is controlled by the density distribution of the interface states in equilibrium with the semiconductor and the applied voltage. In nonideal Schottky diodes, the values of the voltage drops across the interfacial layer, the depletion layer and the bulk resistance are given in terms of the bias dependent ideality factor, n, different from those in literature. These values are determined by a formula obtained for and V, by means of change of the interface charge with bias.

An experimental explanation of the forward bias Capacitance-frequency plots for intimate or MIS SBDs with perfect or imperfect ohmic back-contact has been made. It has been shown that there is no excess capacitance that could be ascribed to the interface states or minority carrier at the intimate SBDs (that is, without interfacial layer) with the perfect ohmic back contact (low-resistance). It has been found that the excess capacitance is only measurable at SBDs with imperfect back contacts or with an interfacial layer which separates the interface states from the metal. It has been found that excess capacitance can be generated by varying the resistance or quality of the back-ohmic contact to the bulk semiconductor substrate, that is, the density of minority carriers that are injected by the Schottky contact depends sensitively on the properties of the ohmic back-contact. Again, it has been seen that the excess capacitance has appeared owing to the interface states plus minority carriers in MIS SBDs with imperfect back contacts. Thus, it has been concluded that the excess capacitance at nonideal Schottky contacts has been caused not only by the interface states but also by the minority carriers or by the interface states plus minority carriers due to the poor frontside or poor backside contacts. Thereby, it has been experimentally shown that every forward bias C-f plots with excess capacitance cannot be used to extract the results related to the interface states.

The present study was carried out to evaluate the hepatoprotective effect and antioxidant role of infusion prepared from linden flowers (LF) against ethanol-induced oxidative stress. The hepatoprotective and antioxidant role of the plant's infusion against ethanol-induced oxidative stress was evaluated by measuring liver damage serum biomarkers, aspartate aminotransferase (AST), alanine aminotransferase, lactate dehydrogenase (LDH), total protein, total albumin, and total cholesterol level; ADS such as GSH, GR, SOD, GST, CAT and GPx, and MDA contents in various tissues of rats. Rats were divided into four experimental groups: I (control), II (20 % ethanol), III (2 % LF), and IV (20 % ethanol + 2 % LF). According to the results, the level of serum marker enzymes, AST and LDH, was significantly increased in group alcohol and group LF as compared to control group, whereas decreased in group IV as compared to ethanol group. With regard to MDA content and ADS constituents, MDA contents of alcohol group in all tissues, except for erythrocytes and heart, and in brain, kidney, and spleen of LF group significantly increased compared to control group, whereas LF beverage extract supplementation did not restore the increased MDA towards close the control level. In addition, while ethanol caused fluctuation in antioxidant defense system constituents level as a result of oxidative stress condition in the rats, it could have not been determined the healing effects of the LF against these fluctuations. The results indicated that LF beverage extract could not be as important as diet-derived antioxidants in preventing oxidative damage in the tissues by reducing the lipid oxidation or inhibiting the production of ethanol-induced free radicals in rats.

The aims of our study were the evaluation of the hepatoprotective effect and antioxidant role of walnuts against ethanol-induced oxidative stress. The hepatoprotective and antioxidant role of the walnuts supplementation feed against ethanol-induced oxidative stress were evaluated by measuring liver damage serum marker enzymes; aspartate aminotransferase (AST); alanine aminotransferase (ALT); gamma glutamyl transpeptidase (GGT); lactate dehydrogenase (LDH); and antioxidant defense systems such as reduced glutathione, glutathione reductase, superoxide dismutase, glutathione-S-transferase, catalase, and glutathione peroxidase and Malondialdehyde (MDA) content in various tissues of rats. Rats were divided into six experimental groups: I (control), II (20 % ethanol), III (10 % walnuts), IV (20 % ethanol + 10 % walnuts), V (5 % walnuts), and VI (20 % ethanol + 5 % walnuts). According to the results, the biochemical analysis showed a considerable increase in the serum aspartate AST, ALT, GGT, and LDH in the group II as compared to that of group I, whereas decreased in group IVas compared to that of group II. In addition, administration of walnuts supplementation restored the ethanol-induced imbalance between MDA and fluctuated antioxidant system toward close control group particularly in the tissues. The results indicated that walnuts could be as important as diet-derived antioxidants in preventing oxidative damage in the tissues by reducing the lipid oxidation or inhibiting the production of ethanol-induced free radicals in rats.

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