Beryllium induced toxic manifestations in rat brain: Dose and duration dependent study

Exposure to beryllium causes bronchitis, bronchiolitis, chronic pulmonary granulomatosis, pneumonitis, hepatic and nephrotoxicity. In the present study, we carried out a dose and duration dependent study on beryllium induced toxic manifestations in rat brain. For dose dependent experiment, four groups of female albino rats were challenged with beryllium nitrate at 0.25, 0.50, 0.75 and 1.0 mg/kg, i.p. daily for 2 weeks, respectively. Similarly, for duration dependent study, animals were challenged with 1.0 mg/kg, i.p. dose of beryllium nitrate for 2, 4 and 6 weeks, respectively. Behavioural, biochemical and histopathological variables were performed to evaluate toxic effects of beryllium. Beryllium exposure decreased body weight, decreased motor coordination and increased anxiety level in dose and duration dependent manner. Total RBCs and hemoglobin content were decreased after beryllium intoxication. Serum bilirubin, creatinine, triglyceride, AST and ALT content were increased after beryllium intoxication, whereas ALP content was decreased in dose and duration dependent manner. Peroxidative damage was noticed in different parts of brain in dose and duration dependent manner. Beryllium administration altered histoarchitecture of brain cortex in same manner. In dose dependent study, maximum alterations in various parameters were evident at 1.0 mg/kg dose, and also it showed toxic consequences of beryllium in a duration dependent manner. Thus, exposure of 1.0 mg/kg dose of beryllium for 4 weeks duration was found to be most suitable for further studies of assessment of therapeutic agent against beryllium induced neurotoxicity.

Protective potential of Moringa oleifera Lam. along with curcumin and piperine against beryllium-induced alterations in hepatorenal biochemistry and ultramorphology in rats

Moringa oleifera Lam. (Moringaceae) is a medicinally important plant, used as traditional medicine all over the world particularly in South Asia and India. Hydroalcoholic (50% v/v) root extract of M. oleifera (150 mg/kg, p.o.) with piperine (2.5 mg/kg, p.o), or curcumin (5.0 mg/kg, p.o.) was administered daily for 1 week in Female Wistar albino rats against beryllium toxicity (1.0 mg/kg, i.p. daily for 5 weeks). Beryllium altered hepatorenal function and enhanced the leakage of AST, ALT, and LDH, depleted SALP activity, and increased the level of urea, uric acid, creatinine, triglyceride and total cholesterol in the blood. Beryllium altered tissue biochemical parameters by a decrease in SDH, ALPase, ATPase activities, and increased ACPase activity, depleted hemoglobin and ALAD activity with an increase in ALAS activity and serum bilirubin. A significant amount of beryllium deposited in the liver, kidney, spleen, and bones. M. oleifera with curcumin showed better antitoxic potential by reversal of hepatorenal function towards normal and restored the activity of SDH, ALPase, ATPase, ACPase, and hemoglobin level normal. M. oleifera with curcumin effectively mobilized beryllium from the body and restored ultrastructure of liver and kidney. It was concluded that curcumin enhances the antitoxic potential of M. oleifera root extract and reduces beryllium body burden in rats.

Protective effects of propolis on inorganic mercury induced oxidative stress in mice.

Protective potential of propolis was evaluated against mercury induced oxidative stress and antioxidant enzymatic alterations in mice liver. Exposure to mercuric chloride (HgCl2; 5 mg/kg; ip) induced oxidative stress by increasing lipid peroxidation and oxidized glutathione level along with concomitant decrease in glutathione and various antioxidant enzymes. Mercury intoxication deviated the activity of liver marker enzymes in serum. Conjoint treatment of propolis (200 mg/kg; po) inhibited lipid peroxidation and oxidized glutathione level, whereas increased glutathione level. Activities of antioxidants enzymes, i.e., superoxide dismutase, catalase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase were also restored concomitantly towards control after propolis administration. Release of serum transaminases, alkaline phosphatase, lactate dehydrogenase and y-glutamyl transpeptidase were significantly restored towards control after propolis treatment. Results suggest that propolis augments the antioxidants defense against mercury induced toxicity and provides evidence that it has therapeutic potential as hepatoprotective agent.

Effect of propolis extract on acute carbon tetrachloride induced hepatotoxicity.

Ethanolic extract of propolis was administered to rats intoxicated by carbon tetrachloride. Administration of bolus dose of CCl4 (1.5 ml/kg, ip) resulted in elevation of serum transaminases and serum alkaline phosphatase activities. Levels of hepatic lipid peroxidation were significantly increased. On the contrary, there was significant decrease in hepatic reduced glutathione level. The propolis extract (100 and 200 mg/kg, po) exhibited recoupment in both pre- and post-treatment (prophylactic and curative studies) of biochemical changes induced by CCl4. The post treatment of 200 mg/kg, po extract showed most significant hepatoprotective effect. Histopathological studies showed damage in hepatocytes and disturbed chord arrangement after toxicant administration. Propolis extract (200 mg/kg, po) was found to be more effective in restoring CCl4 induced histopathological alterations.

Effect of propriety herbal formulation against chronic carbon tetrachloride induced hepatotoxicity.

Efficacy of propriety herbal formulation (PHF) against carbon tetrachloride (CCl4) induced liver damage was investigated in adult rats. Administration of CCl4 (0.2 ml/kg; i.p.) twice a week for 12 weeks resulted in significant elevation in serum transaminases activity. Level of reduced glutathione was significantly decreased. On the contrary, significant elevation was found in the hepatic lipid peroxidation level. Proliferation of fibroblast replaced the hepatic parenchyma cells in focal areas. Cell organelles like mitochondria, endoplasmic reticulum and nucleus showed severe degeneration after CCl4 exposure. PHF was effective in restoring the CCl4 induced biochemical and histological ultrastructural changes.