Oral Paper

         Mycology & Phycology

Pharmacological intervention of Russula sp.

Presenting Author
Muhammad Hanif
Description
Mushrooms possess therapeutic effects since ages due to biologically active compounds. Objective: Present research aimed to assess the protective effect of a mushroom Russula sp. BRF 5 on carbon tetrachloride-induced hepatocellular carcinoma in Balb C mice. Biochemical parameters from blood like total protein, total bilirubin content along with some enzymatic activities viz; alanine aminotransferase (ALAT), aspartate aminotransferase (ASAT), lactate dehydrogenase (LDH), alkaline phosphatase (ALP), malondialdehyde (MDA), glutathione (GSH) and catalase in blood plasma were analysed. Results: The induction of carbon tetrachloride CCl4 induced hepatotoxicity caused a highly significant surge (p≤ 0.001) in the activity of ALAT, ASAT, ALP, MDA and LDH while a significant decrease (p≤ 0.001) in GSH and Catalase level of plasma was observed. Mice were treated with CCl4 at a dose of 1ml/kg b.w for disease induction and Russula sp. BRF 5 extract at three different concentrations (1, 2 and 4 mg/ml) to check their effect on some biochemical components as well as enzymatic activities. Russula sp. BRF 5 proved to eradicate the CCl4-induced changes in the enzyme level. The mushroom caused a highly significant rise (p≤ 0.001) in total protein content (6.16±0.4 g/dl) which was lowered to 2.94±0.1 g/dl as compared to control (8.42±0.4 g/dl) after CCl4 administration. Moreover, ALAT, ASAT, ALP, LDH and MDA activity was restored to normal while a decline in bilirubin content (3.34±0.1 mg/dl) was also observed. Hepatic damage caused by CCl4 was obliterated by Russula sp. pre-treatment on mice. Best anticancer potential was recorded for the highest concentration of mushroom extracts at 4 mg/ml. Conclusion: These outcomes revealed that Russula sp. BRF 5 extract ameliorated the damage caused by CCl4 in the mice model, which confirms its protective effects against hepatic damage caused by oxidative as well as non-oxidative mechanisms.