Liver Sections Of Animals Research Articles

Toxicological Profile of the Aqueous Extract of Tectona grandis L.F. (Verbenaceae) Leaves: A Medicinal Plant Used in the Treatment of Typhoid Fever in Traditional Cameroonian Medicine

Tectona grandis (T. grandis) is a medicinal plant widely used in Cameroon to treat typhoid fever and several other diseases. Despite its heavy use for medical purposes, no study has yet been conducted to assess its potentially toxic effects. This study aimed at evaluating the acute and subchronic toxicological profile of Tectona grandis leaf extract in rats. The acute toxicity study revealed neither behavioral disturbances nor death in rats. The lethal dose (DL50) of this extract is greater than 5000 mg/kg body weight. The subchronic toxicity study showed no significant change in weight gain in rats at test doses throughout the treatment period. However, there was a significant decrease in alanine transaminase activity and serum protein levels at all doses. Alkaline phosphatase activity decreased at doses of 30, 90, and 270 mg/kg and increased at the dose of 810 mg/kg body weight. Serum and urinary urea levels increased simultaneously at doses of 270 and 810 mg/kg body weight. Repeated administration of the extract also increased total cholesterol, high-density lipoprotein levels in both sexes were compared to respective controls, and the ratio of high- to low-density lipoprotein was found to be greater than 1 in all animals. However, at the dose of 810 mg/kg, necrosis was observed on the kidney sections and vascular congestion on the liver sections of animals. Aqueous extract of T. grandis did not lead to any adverse effects in rats after acute and subchronic treatment at 30 and 90 mg/kg doses. This extract can, therefore, be used for the formulation of typhoid fever phytomedicine at the therapeutic dose of 30 mg/kg, but before this, chronic and mutagenic toxicity evaluations must be carried out.

Protective Effect of Arabic Gum on liver Injury Experimentally Induced by Gentamycin in Mice

This research was conducted to evaluate the effect of Arabic gum (Ag) on hepatotoxicity induced by gentamycin in mice. Forty adult male Bulb/c mice were used. The animal were divided into four groups (Gs) each group 10 animals. G1 considered as control, G2 treated with gentamycin(40mg/kg/day) for 8 days (i.p.). G3 treated with Ag (10 gm/kg/day) for 8 days administrated orally. Then G4 treated with both gentamycin and Ag for 8 days. Biochemically, the results showed a significant decrease in levels of serum ALT and AST in G4 as compared with G2 . Moreover, serum Glutathione (GSH) in G4 also elucidate a significant increasing in its level, as well as a significant decrease in levels of malondialdihyde (MDA). Histopathologically, liver sections of animals in G4 revealed an ameliorative effects of Ag as compared with its compatible tissue sections of G2. Liver of mice treated with Ag (G3) showed an apoptosis in hepatocytes. In conclusion, treatment of hepatotoxicity by Arabic gum , showed melioration in histopathological changes in hepatic tissues in addition to have ability for induction of apoptosis and meliorating liver picture.

Intrahepatic Distribution of Plutonium in Beagles

GEARHART, J. M., DIEL, J. H., AND MCCLELLAN, R. O. Intrahepatic Distribution of Plutonium in Beagles. Radiat. Res. 84, 343-352 (1980). Autoradiographs of liver tissue sections were used to study the microscopic distribution of plutonium both by degree of uniformity and by association with morphological structures and cell types. The distribution of plutonium deposited in liver as a result of gradual introduction into blood by absorption from lung was compared with the distribution of Pu after acute intravenous injection of a soluble form of Pu. Beagle dogs were exposed by inhalation to a 238PuO2 aerosol or by intravenous injection to 238pu or 239Pu-citrate and the distribution of Pu in liver was measured (t = 64-1553 days) after exposure. Random distribution of plutonium at early times after exposure was changed to clustering of activity at times beyond 2 years after inhalation exposure. Plutonium which initially was distributed an equal distance from central veins and portal triads moved closer to central veins. The distribution of Pu in liver at the cellular level from high levels of Pu exposure was not the same as that at lower levels of exposure such as those most likely to be encountered by man. Particles were found in liver sections of animals that died by 1350 days after exposure by inhalation to a mean initial lung burden of 0.97 tLCi/kg body wt. This indicated that for high initial lung burdens, particle transfer can occur. At low levels of exposure, distributions of plutonium deposited in liver after translocation from lung and after intravenous injection were similar for at least 4 months after exposure.