Medicinal plants are unique in having the ability to produce diverse chemical compounds with remarkable biological activities. Investigations of medicinal plants resulted in the discovery of a large number of bioactive compounds with excellent therapeutic properties. Solanum surattense, a perennial wild growing medicinal herb, is widely used in the traditional medicine. Exhaustive literature availability reveals the presence of phytochemical compounds from different plant parts like roots, stem, leaves, fruits, and seeds reported to possess a wide range of pharmacological activities like hepatoprotective, cardioprotective, antiasthmatic and mosquito repellents properties. Intensive investigation on phytochemical constituents resulted in isolation of alkaloid and steroidal compounds solasonoine, solamargine, campesterol, and diosgenin. Evaluation of therapeutic activity of isolated compounds proved as potent ones with reference to the standard. Current literature on the pharmacological activity of S. surattense confirms the scientific validation of folklore claims and its traditional use to cure various ailments. Present review is undertaken to summarize all the available information on pharmacological activities, which provide a baseline support for further exploration of its unexplored therapeutic effects like immunomodulation, antipiles activity, antianaphylactic activity, and sexual behavior claimed by folklore.

Ammonia is an important source of nitrogen metabolism and it is necessary for synthesis of protein and amino acids. An excessive level of ammonia leads to disturbance in the physiological functions of the body. High concentrations of ammonia enter into the body, because of environmental pollution, urea cycle disorders, liver failure and ingestion of ammonium salts cause physiological disturbance and damage of organs. The present study is to investigate the possibilities of the protective role of Selenium in Ammonium Sulphate (AS)-induced stress in the rat brain and liver. Rats were divided into four groups (six animals in each group). Group I (GI) is served as control, Group II (AS) rats received 18.3 mg/kg b.w of ammonium sulphate via intraperitonially (i.p) injection, Group III (Ss) rats administered with Sodium selenite (0.3 mg/kg b.wi.p) and Group IV (AS + Ss) treated with both of AS (18.3 mg/kg bwi.p) plus Ss (0.3 mg/kg b.wi.p). Acute intoxication of AS treated rats has shown that significantly decreased levels of antioxidant enzymes; namely Superoxide dismutase (SOD), Catalase (CAT), Glutathione peroxidase (GPx), and increased levels of Xanthine oxidase (XOD) levels in brain and liver tissues. Treatments with Ss reversed the ASinduced alteration of antioxidant defence enzyme levels.Selenium administration might be scavenging the excess of ammonium ions and significantly prevent the oxidative stress in liver and brain.

Objective: Intention of the present study is to investigate the protective role of zinc against ammonium sulfate (AS) toxicity in renal tissue by evaluating certain biochemical activities of albino rats. Methods: Rats were divided into four groups, namely control, ammonia, zinc, and ammonia + zinc. Rats were exposed to AS (18.3 mg/kg body weight) or zinc chloride (4 mg/kg body weight) or both through intraperitoneally for 7-day experimentation with 24-h time interval. Results: AS-administered rats showed significant increased levels of ammonia, urea, glutamine, glutamine synthetase, free amino acids, and lactate dehydrogenase and decreased levels of total proteins, pyruvate, succinate dehydrogenases, malate dehydrogenase, and biochemical activities when compared with control. Supplementation of zinc mitigated AS-induced oxidative stress and restored all the biochemical parameter activities. Zinc administered to normal rats did not exhibit any significant changes in any of the parameters studied. Conclusion: From the study, it concluded that zinc cotreatment with AS has effectively recovered the mitochondrial enzyme activities and ammonia metabolic biochemical parameters in renal tissue of rat treated with AS.

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