Comparative Bioactivity Evaluation of Chemically Characterized Essential Oils Obtained from Different Aerial Parts of Eucalyptus gunnii Hook. f. (Myrtaceae).

Essential oils (EOs) obtained by hydro-distillation from different parts of twigs (EOT), leaves (EOL), and fruits (EOF) of Eucalyptus gunnii Hook. f. were screened for their chemical composition, insecticidal, repellence, and antibacterial properties. Based on GC and GC/MS analysis, 23 constituents were identified across the twigs, leaves, and fruits, with 23, 23, and 21 components, respectively. The primary significant class was oxygenated monoterpenes (82.2-95.5%). The main components were 1,8-cineole (65.6-86.1%), α-terpinyl acetate (2.5-7.6%), o-cymene (3.3-7.5%), and α-terpineol (3.3-3.5%). All three EOs exhibited moderate antibacterial activities. EOL was found to have higher antibacterial activity against all tested strains except Dickeya solani (CFBP 8199), for which EOT showed more potency. Globally, Dickeya solani (CFBP 8199) was the most sensitive (MIC ≤ 2 mg/mL), while the most resistant bacteria were Dickeya dadantii (CFBP 3855) and Pectobacterium carotovorum subsp. carotovorum (CFBP 5387). Fumigant, contact toxicity, and repellent bioassays showed different potential depending on plant extracts, particularly EOT and EOL as moderate repellents and EOT as a medium toxicant.

Nomega-nitro-L-arginine methylester ameliorates myocardial toxicity induced by doxorubicin.

The effects of Nomega-nitro-L-arginine methylester (L-NAME) and L-arginine on cardiotoxicity that is induced by doxorubicin (Dox) were investigated. A single dose of Dox 15 mg/kg i.p. induced cardiotoxicity, manifested biochemically by a significant elevation of serum creatine phosphokinase (CPK) activity [EC 2.7.3.2]. Moreover, cardiotoxicity was further confirmed by a significant increase in lipid peroxides, measured as malon-di-aldehyde (MDA) in cardiac tissue homogenates. The administration of L-NAME 4 mg/kg/d p.o. in drinking water 5 days before and 3 days after the Dox injection significantly ameliorated the cardiotoxic effects of Dox, judged by the improvement in both serum CPK activity and lipid peroxides in the cardiac tissue homogenates. On the other hand, the administration of L-arginine 70 mg/kg/d p.o. did not protect the cardiac tissues against the toxicity that was induced by the Dox treatment. The findings of this study suggest that L-NAME can attenuate the cardiac dysfunction that is produced by the Dox treatment via the mechanism(s), which may involve the inhibition of the nitric oxide (NO) formation. L-NAME may, therefore, be a beneficial remedy for cardiotoxicity that is induced by Dox and can then be used to improve the therapeutic index of Dox.

Morphology of the egg shell and the developing embryo of the Red Palm Weevil, Rhynchophorus ferrugineus (Oliver).

The harvested eggs of Rhynchophorus ferrugineus are ovo-cylindrical shaped, averaged 1.09 mm in length and 0.43 mm in width, with ratio of [Formula: see text] 4.42. The chorionic layer of electron dense material is seen covering the exochorion structure of the eggs. The egg main body chorion exhibits a polygonal pattern and architecture surface of the egg is supported by a system of irregular interconnecting grooves. The micropylar apparatus of the eggs of the Red Palm Weevil, R. ferrugineus is described in the present study for the first time. Two micropylar openings are found closed to the center of the posterior wide pole of the egg. Each micropylar opening presents a single small orifice and its surrounding chorion is porous and densely set with tiny projections allowing the spermatozoa to penetrate the egg. Respiratory aeropyles are distributed on the borders of reticulations in the area chorionic surface of egg capsule. The hatching region is detected on the anterior part at the opposite side of the egg. Changes in the appearance and shape of R. ferrugineus eggs as well as the incidence of embryonic development are observed.

Thymoquinone supplementation reverses acetaminophen-induced oxidative stress, nitric oxide production and energy decline in mice liver.

This study was undertaken to evaluate the protective effect of thymoquinone (TQ) against acetaminophen-induced hepatotoxicity. Mice were given TQ orally at three different doses (0.5, 1 and 2mg/kg/day) for 5 days before a single hepatotoxic dose of acetaminophen (500 mg/kg i.p.). TQ supplementation dramatically reduced acetaminophen-induced hepatotoxicity, in a dose-dependent manner, as evidenced by decreased serum alanine aminotransferase (ALT) activities. Acetaminophen (500 mg/kg i.p.) resulted in a significant increase in serum ALT and total nitrate/nitrite, hepatic lipid peroxides and a significant decrease in hepatic reduced glutathione (GSH) and ATP in a time-dependent manner. Interestingly, supplementation of TQ (2mg/kg/day) for 5 days before acetaminophen administration resulted in reversal of acetaminophen-induced increase in ALT, total nitrate/nitrite, lipid peroxide and a decrease in GSH and ATP. Moreover, TQ did not affect acetaminophen-induced early decrease in hepatic GSH indicating lack of the effect on the metabolic activation of acetaminophen. In conclusion, TQ is effective in protecting mice against acetaminophen-induced hepatotoxicity possibly via increased resistance to oxidative and nitrosative stress as well as its ability to improve the mitochondrial energy production.

Protective effect of aminoguanidine against paraquat-induced oxidative stress in the lung of mice.

The effect of aminoguanidine (AG) against toxicity of paraquat (PQ), an oxidative-stress inducing substance, in mice was investigated. A single dose of PQ (50 mg/kg, i.p.) induced lung-toxicity, manifested by significant decrease of the activity of angiotensin converting enzyme (ACE) in lung tissue indicating pulmonary capillary endothelial cell damage. Lung toxicity was further evidenced by significant decrease of total sulfhydryl (-SH) content and significant increase in lipid peroxidation measured as malondialdehyde (MDA) in lung tissues. Oral pretreatment of mice with AG (50 mg/kg) in drinking water, starting 5 days before PQ injection and continuing during the experimental period, ameliorated the lung toxicity induced by PQ. This was evidenced by a significant increase in the levels of ACE activity, a significant decrease in lung MDA content and a significant increase in the total sulfhydryl content 24 h after PQ administration. Moreover, pretreatment of mice with AG leads to an increase of the LD(50) value of paraquat. These results indicate that AG is an efficient cytoprotective agent against PQ-induced lung toxicity.

Effects of thymoquinone on antioxidant enzyme activities, lipid peroxidation and DT-diaphorase in different tissues of mice: a possible mechanism of action.

The present investigation focused, firstly, on the effects of oral administration of thymoquinone (TQ) on antioxidant enzyme activities, lipid peroxidation and DT-diaphorase activity in hepatic, cardiac and kidney tissues of normal mice. Superoxide dismutase (SOD; E.C:1.15.1.1), catalase (CAT; E.C:1.11.1.6), glutathione peroxidase (GSH-Px; E.C:1.11.1.9), glutathione-S-transferase (GST; E.C:2.5.1.18), and DT-diaphorase (E.C:1.6.99.2) enzyme activities in each tissue type were determined. Treatment of mice with the different doses of TQ (25, 50 and 100 mg kg(-1) day(-1) orally) for 5 successive days, produced significant reductions in hepatic SOD, CAT and GSH-Px activities. In addition cardiac SOD activity was markedly inhibited with the higher doses of TQ, (namely 50 and 100 mg kg(-1)). Moreover, TQ (100 mg kg(-1)) significantly reduced hepatic and cardiac lipid peroxidation as compared with the respective control group. Conversely, TQ (50,100 mg kg(-1)) and TQ (100 mg kg(-1)) enhanced cardiac and renal DT-diaphorase activity respectively. However, the selected doses of TQ neither produced any change in GST activity nor influenced reduced glutathione content in all tissues studied. TQ was tested, secondly, as a substrate for hepatic, cardiac and renal DT-diaphorase of normal mice in the presence of NADPH. Kinetic parameters for the reduction of TQ to dihydrothymoquinone (DHTQ) indicated that DT-diaphorase of different tissues can efficiently reduce TQ to DHTQ. K(m) and V(max) values revealed that hepatic DT-diaphorase exhibited the higher values, while the lower values were associated with renal DT-diaphorase. TQ and DHTQ were tested, thirdly, as specific scavengers for superoxide anion (generated biochemically) or as general scavengers for free radicals (generated photochemically). The results revealed that TQ and DHTQ acted not only as superoxide anion scavengers but also as general free radical scavengers. The IC(50) for TQ and DHTQ in biochemical and photochemical assays were in the nanomolar and micromolar range respectively. Our data may explain at least partly the reported beneficial in vivo protective effects of TQ through the combined antioxidant properties of TQ and its metabolite DHTQ.

Protective effect of arabic gum against acetaminophen-induced hepatotoxicity in mice.

Overdose of acetaminophen, a widely used analgesic drug, can result in severe hepatotoxicity and is often fatal. This study was undertaken to examine the effects of arabic gum (AG), which is commonly used in processed foods, on acetaminophen-induced hepatotoxicity in mice. Mice were given arabic gum orally (100 g l(-1)) 5 days before a hepatotoxic dose of acetaminophen (500 mg kg(-1)) intraperitoneally. Arabic gum administration dramatically reduced acetaminophen-induced hepatotoxicity as evidenced by reduced serum alanine (ALT) and aspartate aminotransferase (AST) activities. Acetaminophen-induced hepatic lipid peroxidation was reduced significantly by arabic gum pretreatment. The protection offered by arabic gum does not appear to be caused by a decrease in the formation of toxic acetaminophen metabolites, which consumes glutathione, because arabic gum did not alter acetaminophen-induced hepatic glutathione depletion. Acetaminophen increased nitric oxide synthesis as measured by serum nitrate plus nitrite at 4 and 6 h after administration and arabic gum pretreatment significantly reduced their formation. In conclusion, arabic gum is effective in protecting mice against acetaminophen-induced hepatotoxicity. This protection may involve the reduction of oxidative stress.