Rat osteoblasts were isolated from the 21-day fetal rat calvarias. The cells were grown in DMEM plus 10% FBS, and were treated for 24 h. With 10 μmol/L TPEN or 10 μmol/L TPEN supplemented with 10 μmol/L Zn2+ . Apoptosis of osteoblasts were measured by flow cytometry, electron microscopy and DNA fragmentation analyzed by gel electrophoresis. In addition, IP3 production and PKC activity were measured in order to show whether they are involved in apoptosis in osteoblast induced by zinc deficiency. The results showed that 10 μmol/L TPEN could induce apoptosis in osteoblast in 24 h. But cells treated with 10 μmol/L TPEN supplemented with 10 μmol/L Zn2+showed no apoptotic changes in 24 h. TPEN significantly reduced the formation of IP3 and PKC activity after 24 h incubation. No differences were observed between the cells treated with TPEN supplemented with Zn2 + simultaneously and the untreated cells. It can be inferred that apoptosis induced by zinc deficiency may be due to the decreased activity of PKC which is impaired by reduced formation of IP3.
Maize seedlings were cultured in nickel or cadmium contaminated sand treated with α-naphthylacetic acid (NAA). The effects of NAA on nickel and cadmium uptake in roots, shoots, and subcellular fractions (cell wall, nuclei and remained parts of seedling cells) were determined. The data showed growth promotion when NAA was applied at low concentrations and inhibition at high concentrations. Uptake of nickel and cadmium content increased concurrently in roots and shoots. In the subcellular fraction, nickel and cadmium was greatest in the cell wall. The changes in growth had greatest correlation with nickel and cadmium content in the subcellular fraction.
Nicotinamide (NA), a naturally occuring vitamin and a protease inhibitor, has been shown to be effective in treating some skin ailments. It inhibits cell proliferation and induces cell differentiation. This report shows the effects of NA on mouse skin tumor development and on the critical events involved in this process. NA reduced tumor growth, inhibited the 12-O-tetradecanoylphorbol- 13-acetate (TPA) induced ornithine decarboxylase activity, but induced the transglutaminase activity which was inhibited by TPA under different experimental conditions.The effects of NA on ornithine decarboxylase (ODC) and transglutaminase (TG) indicated that nicotinamide (NA) probably programmmed the cells for their death in the natural course of time, I.e. Programed cell death. This observation indicates that NA might be a better agent for the detailed study and for the better use in prevention of cancer alone or in combination with other drugs.
Toxicological Impact of Benzenehexachloride on the Behaviour and Neuropathology of Heteropneustes fossilis.
Organochlorine pesticides are widely used in the vast agricultural fields of Assam, India. Runoffs from treated fields contaminates nearby bodies of water with organochlorine compounds, which are neurotoxic to the ichthyofouna. The present work was designed to study the effect of bezenehexachloride on the behaviour and histopathology of Heteropneuates fossilis, as an experimental model.The experimental fish were exposed to different concentrations of the pesticide for 72 hours. After exposure, the fish exhibited various behavioural changes. Histopathological examination of brain tissue revealed cytopathic and gross histopathological alteratios, including necrosis and infractional changes. These results are consistent with the finding that organochlorides cause neurotoxic effects.
This study describes the use of algae as potential bioindlieators of pollution eontaining industrial metals. Phytoplanktonie algae varied with waste type and with enviromnental and growth conditions.In water samples containing ceramic waste Euglenophyta speeies and Cyclotella sp. (Bacillariophyta) were determined as potential indicator species of pollution, while in sample containing metallic waste, Cyclotella sp. Was most dominant. Under laboratory growth conditions, phytoplankton collected from a major stream of the Nile River were eultivated by using Algal Growth Bottle Test (EPA, 1972). This revealed that Scenedesmus sp., Actinastrum hantzschii (Chlorophyta), Oscillatoria limnetica (Cyanophyta) and Nitzschia linearis (Bacillariophyta) were also potential indicators of pollution.
Toxic effects of inhaled sulfur mustard (SM) on the histology of visceral organs was investigated by exposing mice to 84.6mg/m3 for 1 h duration, using controlled single exposure conditions. A progressive fall in body weight from third day onwards was noticed. Light microscopic examination of the pulmonary tissue of these animals at 6 h post exposure revealed that the tracheobronchial epithelium remained intact, but was infiltrated by inflammatorv cells. By 24 h post exposure, the mucosecretory cells were destroyed. The inflammatory reaction was maximum at 48 h. Bv 7th day post exposure there was swelling and vacuolation of lung parenchymal cells and thrombi formation. In addition SM caused congestion and hemorrhage at alveolar level. SM also caused granulovacuolar degeneration with perinuclear clumping of the cytoplasm of hepatocytes and renal parenchymal cells. Renal lesions were characterized by congestion and hemorrhage. Among visceral tissues, maximum atrophy was observed in spleen. Distribution of lesions increased with post exposure period. The maximum lesions were observed at 7th day post-exposure.
The influences of the calmodulin antagonist chlorpromazine (CPZ), and calcium chanmel blocker nimodipine (NLMO) and their combination on cadmium (Cd) poisoning of mice were studied.A series of biochemical parameters including urinary enzyme activities, blood and urine Cd levels, metallothionein (MT) contents in liver and kidney, hepatic ultrastructure and Ca2+ -Mg2- AT Pase activitv in erythrocyte membrane were determined. Animal models for Cd poisoning were established by peritoneal injection of 1/5 LD50 CdCl2. The experimental groups were protected by administration of CPZ, NIMO and CPZ and NIMO in combination I h before the injection of CdCl2. Five days later, samples were collected for analysis. The data showed that CPZ could protect kidney tissue against Cd-induced damage, as the urinary y-glutamyl-traspeptidase (γ-GT) and N-acetyl-β-D-glucosaminidase (NAG) activities were reduced significantly. There was neither evidence of the protective effect of NIMO on kidney tissue nor an indication of a synergistic effecf of CPZ and NIMO.Both CPZ and NIMO showed a considerable protective effect against the decrease in Ca2+ -Mg2+ AT-Pase activity, and a synergistic action was observed. Cd content in blood was reduced significantly by CPZ or the combination of CPZ and NIMO, but elevated by NIMO. Both CPZ and NIMO considerably increased MT contents in livers and kidneys and ameliorated damaged to the hepatic ultrastructures caused by Cd. The results indicated that these inhibitors could protect mice against the toxic effects of Cd in liver and kidney tissues, while CPZ was more efficient than NIMO. The combination of CPZ and NIMO excrted a synergistic action. The protective action of these two drugs might be relevent to the function of MT.
The hypoglycemic activity of an ethanol extract of Hibiscus rosa-sinensis was studied in glucose located rats. After a single dose of the extract, a slight but insignificant hypoglycemic effect was observed at 30 and 90 min. At 120 min it was mild but significant. After repeated administration of the extract (once a day for seven consecutive days) a statistically significant (P ＜ 0.001) reduction in blood glucose levels was observed at 30, 90 and 120 min after glucose loading. The average hypoglycemic activity, after repeated administration of 250 mg kg- 1 leaf extract was 81 % , under similar conditions average activity of tolbutamide was 96% . At 250 mg@ kg- 1 the efficacy of the extract was found to be 84% of tolbutamide ( 100 mg@ kg- 1 ). Repeated treatment of animals either with tolbutamide a sulphonylurea or H. Rosa-sinensis caused a 2-3-fold improvement in glucose tolerance as compared to those receiving only once. These data suggest that the leaf extract acts like tolbutamide and the mechanism of action may be a stimulation of pancreatic beta cells to produce more insulin or an increase of the glycogen deposition in liver. It appears that the active principle in the tested extract has the sulphonylurea skeleton in which -SO2-NH-CO- group and the substituents (S1 and S2 ) may be the possible active sites responsible for its hypoglycemic activity.