Абстрактный

Estimation of phenol & flavonoid and evaluation of antioxidant potential of methanolic fruit extract of Solanum nigrum L.

Heena Shabnam. H

Cells are regarded as the basic structural and functional unit of every organism. In contrast, it is believed that life has originated from basic chemicals by free radicals, largely initiated by ionising radiation from sun. Paradoxically, the same reactions creating life are also responsible for many diseases, aging and death, simply called oxidative stress mediated diseases which is the focus of this study. In this regard, a free radical is known as a molecule or molecular fragment that contains one or more unpaired electrons in its outer orbital. Oxiadative reactions ensure that the molecular oxygen is completely reduced to water. The products of the partial reduction of oxygen are highly reactive called Reactive Oxygen Species (ROS). The characteristics of ROS include extreme reactivity which on generation of ROS by chain reaction causes damage to various tissues resulting in various metabolic disorders linked to cancer and neurodegenerative diseases such as Memory loss, Alzhemiers disease, Chronic Inflammatory diseases, Cardiovascular diseases, Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) etc.. As most of the study focus on the whole plant, leaves and ripe berries of Solanum nigrum L., there are only few reports about the bioactive ingredients of unripe berries (Eltayeb et al, 1997, Jagadeeshan et al, 2017). The study reveals that phytochemicals present in the methanolic fruit extract of Solanum nigrum L. unripe berries plays an important role in scavenging free radicals. The assays such as DPPH assay, Metal chelating assay, Hydroxyl assay, Gallic acid assay for phenol estimation and Quercetin assay for flavonoid estimation, showing potential antioxidant activity in a concentration dependent manner. Hence, the unripe fruit of the Solanum nigrum L. could be used as the antioxidant supplement for treating oxidative stress mediated cell damage.