Effect of a polyherbal formulation, Ambrex, on butylated hydroxy toluene (BHT) induced toxicity in rats.

Effect of polyherbal formulation Ambrex was evaluated in butylated hydroxytoluene (BHT) induced toxicity of lungs and liver in rats. Toxicity was produced by administering BHT (500 mg/kg/day) for 3 days. Lung damage was evidenced by elevated levels of broncho alveolar lavage fluid (BAL) parameters such as protein, lactate, lactate dehydrogenase (LDH), alkaline phosphatase (ALP), acid phosphatase (ACP) and glucose-6-phosphate dehydrogenase (G6PDH). Liver damage was proved by elevated levels of serum protein and markers such as LDH, ALP, aspartate amino transferase (AST), alanine amino transferase (ALT), decreased level of lipid peroxides (LPO) in serum and glutathione (GSH) in liver. Administration of aqueous suspension of Ambrex (50 mg/kg orally) retained these elevated levels of BAL-protein, lactate, LDH, ALP, ACP, G6PDH and serum-protein, LDH, ALP, AST and ALT at near normal values. Decreased level of liver GSH was retained at near normalcy in Ambrex pretreated BHT-administered animals. There was no change in liver LPO in all the four groups.

Pulmonary phospholipid changes induced by butylated hydroxy toluene, an antioxidant, in rats.

Butylated hydroxy toluene (BHT), 800 mg/kg body weight, dissolved in corn oil and administered (ip) in a single injection to male rats, damaged the lung as indicated by an increase in lavage ACE, protein and LDH and caused a significant increase in phospholipid, particularly, phosphatidyl choline (PC) in lung lavage and extracellular surfactant. The plasma lecithin cholesterol acyl transferase (LCAT) activity was inhibited leading to an increase in serum phospholipids and phosphatidyl choline. The results indicate that BHT-induced lung phospholipidosis may be attributed to an increase in surfactant phospholipids and/or due to the leakage of plasma phospholipids through damaged capillary membrane.