The metabolic fate of fenitrothion, O,O-dimethyl-O-(3-methyl-4-nitro phenyl) phosphorothioate, was investigated in rat tissues during the first 24 hours following the intramuscular administration of the pesticide in the animal. High performance liquid chromatography (HPLC) of the pesticide and its metabolites formed in liver, kidney and brain showed the time-dependent sequential conversion of the pesticide into three major metabolites. These metabolites were separated and purified to homogeneity by HPLC and characterized by IR spectroscopy as O,O-dimethyl-O-)3-methyl-4-aminophenyl) phosphorothioate (metabolite I), O,O-dimethyl phosphorothioate (metabolite II), and O,O-dimethylphosphate (metabolite III). These results indicated reduction of the nitro group in fenitrothion aas the first step, followed by the hydrolytic cleavage of the P-O-aryl bond in metabolite I and the oxidative desulphurylation of metabolite II. Fenitrothion was found to induce ultrastructural changes in liver cells especially after 12 h exposure nuclear membrane was completely distorted, nuclear intactness was totally lost and smooth endoplasmic reticulum and Golgi apparatus were abnormally enlarged. In 24 h, however, the regeneration of the nuclear material was observed.

The biodegradation of fenitrothion O,O-dimethyl-O-(3-methyl-4-nitro phenyl) phosphorothioate was investigated in rat liver after administration of various doses (5 mg/100 g body weight and 20 mg/100 g body weight) in acute treatment and 1 mg/100 g body weight in chronic treatment. High performance liquid chromatography of the pesticide and its metabolites formed in liver in acute treatment showed time-dependent sequential conversion of pesticide into three major metabolites within 24 h. These metabolites were separated and purified to homogenity by HPLC and characterized by IR spectroscopy as O,O-dimethyl-O-(3-methyl-4-amino phenyl) phsophorothioate (metabolite 1), O,O-dimethyl phosphorothioate (metabolite II) and O,O-dimethyl phosphate (metabolite III) in the fi rst dose (5 mg/100 g body weight). Metabolite II was found to be different in the second dose (20 mg/100 g body weight) and identified as O,O-dimethyl O-3-methyl-4-amino phenyl phosphate. The results with the fi rst dose indicated reduction of the nitro group in fenitrothion as step I followed by hydrolytic clevage of the P-O-aryl bond in metabolite I and oxidative desulphurylation of metabolite II. At higher dose (20 mg/100 g body weight) oxidative desulphurylation takes place as step II followed by hydrolysis of metabolite II. The bioaccumulation of fenitrothion within 60 days during chronic treatment showed no metabolite but continuous reduction in fenitrothion concentration, indicating excretion of pesticide and its products in urine and in faeces.

The octadecanoic acid (OA), methyl ester was isolated and characterized from root of fenugreek (T. foenumgraecum) using ethyl acetate (EAC) in hydroponics method. The OA was characterized by TLC & HPTLC and purified by HPLC. The structure and molecular weight (298) of OA was confirmed by GC-MS. The R f value of sample (peak 4) was matched with standard. OA has strong anti-bacterial activity in B. subitlis and P. aeruginousa, where as weak activity in S. aureus and E. coli. Among the tested concentration of in vitro anti-oxidant activity of OA was maximum in 40μl and minimum in 20μl.

Propoxur (Baygon, 2-isopropoxyphenyl N-methylcarbamate) is a carbamate pesticide commonly used against house insects. When the insecticide was administered intramuscularly in rats it was converted to a new metabolite which was found to be present in the serum, liver, kidney and brain 6 h after the administration of the pesticide. The metabolite was purified by high performance liquid to chromatography and comparison of the infrared spectra of Propoxur and the metabolite showed that a deamination reaction was responsible for the formation of the metabolite from the parent pesticide. The pesticide also induced haematological changes such as an increased level of total bilubrin, amylase and glutamic-oxalacetic transaminase and decrease of cholinesterase activity, indicating damage of the liver and nervous system in rats.

Treatment of pyrimethamine with blood plasma in vitro yields a metabolite which is also produced when the drug is administered through intravenous injection in the rat. A thin layer liquid chromatographic method for quantitative and qualitative determination of pyrimethamine and its metabolite in plasma and biological tissues is described.