Prophylactic effect of antioxidants as free radical scavengers in endotoxemia

Oxidative stress plays a key role in sepsis induced by endotoxin lipopolysaccharide [LPS] which is known to enhance the formation of reactive oxygen species [ROS]. In this study, biochemical parameters indicative of hepatic injury and oxidative stress were tested in rat liver following LPS challenge, with or without treatment with the antioxidants alpha lipoic acid [ALA] and Antox [antioxidant drug preparation]. Treatment with LPS alone resulted in a significant [P<0.05] alteration in liver oxidative status observed as elevation in alanine and asparate aminotransferase [ALT and AST] activities, malondialdehyde [MAD, index of lipid peroxidation] level and nitric oxide [NO] concentration. Also, activities of reduced glutathione [GSH]. Superoxide dismutase [SOD] and glutathione peroxidase [GSH-Px] were significantly [P<0.05] reduced in LPS-treated group, as compared to control level. Treatment for seven days with either ALA or Antox prior to or after LPS challenge significantly [P<0.05] decrease ALT, AST, MDA and NO levels when compared to LPS alone. On the other hand, administration of ALA and Antoxa prior to or after LPS treatment significantly increases the activities of GSH, SOD and GSH-Px when compared with LPS treated group. These results indicate that either ALA or Antox may serve as a potentially effective prophylactic agents in alleviating LPS- induced oxidative stress. The beneficial pretreatment effects of the antioxidant against oxidative stress in this study may suggest a potential chemopreventive effect of these compounds in septic prevention

Alpha lipoic acid ameliorate changes occur in neurotransmitters and antioxidant enzymes that influenced by profenofos insecticide

This study was designed to determine whether alpha lipoic acid [ALA] which has been shown to have substantial antioxidant properties would ameliorate some of profenofos insecticide toxic effects. ALA administered [60mg/kg b.w.] to adult female rats for 14 days 1 hour after administration of 1/10 LD50 [45 mg/kg b.w.] and 1/20 LD50 [22.5 mg/kg b.w.] for profenofos insecticide which act as free radical inducer. Neurotransmitters [Dopamine [DA], Norepinephrin [NE], Serotonine [5-HT] and 5-Hydroxy indol acetic acid [5-HIAA]] were estimated in plasma. While malondialdehyde [MDA], reduced glutathione [GSH] level, glutathione-S-transferase [GST] and superoxide dismutase [SOD] activities were determined in liver, kidney and brain. The results revealed an increase in plasma serotonine [5-HT] levels in group of rats intoxicated with low dose of profenofos. A significant increase in MDA level [an indicator for lipid peroxidation] in liver of rats intoxicated with both doses of profenofos was recorded, concurrent with a significant reduction in GSH level and GST and SOD activities in most tested tissues of rats intoxicated with both doses of profenofos. Supplementation with alpha lipoic acid [60 mg/kg b.wt] 1 h after profenofos administration induced some but not complete improvement in all parameters whereas, it induced significant increase in plasma DA and 5-HT while it reduced lipid peroxidation in each of the examined tissues. These results accompanied with improvement in GSH level especially in liver, in addition to GST and SOD activities in some organs. Its effect differ from tissue to another. In conclusion ALA supplementation to profenofos intoxicated rats induced improvement in lipid peroxidation, total glutathione level and glutathione-S- transferase activity

Effect of alpha cypermethrin and/or selenium on plasma neurotransmitters in male albino rats

The present study was undertaken to investigate the role of selenium as an antioxidant on alpha-cypermethrin neurotoxicity in adult male albino rats. This was achieved by observing the changes occurring in the neurotransmitters in plasma. In this study, the animals were treated with 1/10 LD[50] of alpha-cypermethrin insecticide and/or selenium for 14 and 28 days. The data showed a significant increase in plasma norepinephrine [NE] and dopamine [DA] levels with a significant reduction in plasma serotonin [5-HT], 5-hydroxy indole acetic acid [5-HIAA] and acetylcholinesterase [AchE] were recorded. On the other hand, the level of plasma monoamine oxidase [MAO] showed a significant decrease after 14 days of treatment, then increased after 28 days. Combined supplementation of selenium [in drinking water] and alpha-cypermethrin [orally] exhibit the same changes in plasma neurotransmitters compared to alpha-cypermethrin alone. The results indicate that alpha-cypermethrin induced neurotoxicity is mediated by free radical and selenium didn't play a protective role against alpha-cypermethrin induced neurotoxicity

Toxicological impact of lead and/or rodenticide diphacinone I. Changes in bleeding time, body weight, amino acid and protein contents and food and water consumption in albino rats

An observable depression in food consumption accompanied with a decrease of body weight were noticed in animals exposed to lead in various time intervals of the study. Water consumption showed a decrease in initial periods of exposure to lead but it tended to elevate by the 4[th] week of intoxication. This parameter also decreased during the period of diphacinone group and of lead treated animals followed by diphacinone were higher than those of the control group, however liver weights of both treated groups decreased compared to those of controls. Kidney weight did not change due to treatments. Bleeding time increased through the later periods of lead acetate treatment. Exposure of animals to diphacinone preceded by lead acetate for 4 weeks caused futher increase in the bleeding time compared to control or lead treated groups. Animals treated with only diphacinone showed an elongate bleeding time which was longer than those of other experimental groups. Total protein contents decreased significantly in the liver kidney and brain during the second week of intoxication. In contrast serum showed substantial elevations especially during the initial periods of the treatment. Amino acid analysis indicated a general initial decrease in various organs followed by marked elevations by termination of the experiment

Toxicological impact of lead and/or rodenticide diphacinone on albino rats 2-changes in enzyme profile and protein metabolism

The objective of this study is to explore the interaction between lead pollution and the anticoagulant rodenticide, diphacinone, on adult male albino rats through the disturbances occurring in enzyme activities due to these risk factors. Following are the results obtained: Treatment of animals with diphacinone only has resulted in variable effects on various parameters examined where the highest effect was noticed on the kiduey. However, treatment of rats with lead [Pb] before exposure to diphacinone has counteracted most of the toxicological effects of the anticoagulant on the kidney as evidenced from unaltered renal GPT, alkaline phosphtase and brain 5 -nuclcotidasc and Pb concentration. The effect of the anticoagulant on serum constituents was restricted to 5 nucleotidase activity. However, moderate but significant decrease in sGPT activity was also recorded. With respect to alkaline phosphatase [ALP], diphacinone intoxication has no effect on the activity of this enzyme in both serum and brain, whereas it stimulates hepatic enzyme activity and depressed the activity of this enzyme in the kidney. On the other hand, diphacinone intoxication of animals pretreated with Pb for 28 days has resulted in decreases in activity of ALP in both serum and brain, whereas no detectable change occurred in both liver and kidney. Lead concentration underwent significant decreases in various organs examined following diphacinone treatment when compared with the control groups

Toxicological impact of lead poisoning on enzyme profile in some vital organs of albino rats

The present work was performed to investigate the effects of chronic exposure to lead acetate on enzyme profile in liver, kidney and brain in addition to blood serum of adult male albino rats. Lead concentrations were also monitored in tissues of the previously mentioned organs. Results obtained were as follows: Chronic intoxication with lead acetate induced significant elevation in serum aminotransferase enzymes [sGOT and sGPT], however, the latter enzyme was highly affected in response to treatment than sGOT. Conversely, there were significant declines in the activity of' aminotransferases in almost all examined organs with fluctuable magnitudes. Highly significant decline in serum alkaline phosphatase was observed after administration of lead acetate during different time intervals of experimentation. On the other hand, lead acetate has resulted in excitation of alkaline_phosphatase during the early periods of intoxication, whereas by termination of the experiment, the activity of the enzyme tended to decrease significantly especially in the brain and liver. The present data indicated increases in the activity of serum 5' nucleotidase [5'-NT] during various experimental periods, while tissue 5'-NT showed nearly a similar pattern of changes like alkaline phosphatase. Lead concentrations in blood, brain, liver and kidneys are extremely variable during various periods of treatment with lead acetate. With the exception of the blood, all tissues showed upward trends with exposure time, however, marked elevations were noticed in the blood and liver whereas low concentration was observed in the brain