Effect on free radical generation with different anaesthesia.

Reactive oxygen species are a part of the normal physiology of the biological system but their subsequent defence undergoes alteration during diseased conditions. Administration of anaesthesia for surgery may also alter the formation of reactive oxygen species. The present work deals with the comparative status of oxidative stress (lipid peroxidation) and anti-oxidant defence markers (superoxide dismutase and catalase) in blood in 3 groups of 15 patients each receiving halothane, relaxant vecuronium and spinal form of anaesthesia with lignocaine 5% heavy. The results obtained depict that the formation of malonyl dialdehyde as well as decrease in superoxide dismutase and catalase activities was highest in spinal anaesthesia followed by halothane and then relaxant group. Therefore, it seems important to consider the pre-operative anti-oxidant status while administering anaesthesia to such patients in order to provide biologically safe anaesthesia.

Glucose transport in cerebral microvessels during Plasmodium yoelii nigeriensis infection in mice.

Plasmodium yoelii infected cerebral micro vessels of mice registered a significant increase in D-[U-14C] Glucose transport as compared to normal microvessels which was found to be time, temperature and concentration dependent. Metabolic inhibitors galactose, manose, 2-deoxy glucose and D-glucose showed noticeable inhibition of the same.

Status of urea and related enzymes during Plasmodium yoelii infection and pyrimethamine treatment in mice.

Plasmodium yoelii infection alters the hepatic levels of key enzymes of urea cycle, viz.carbamoyl phosphates synthetase (EC 6.3.4.16) and ornithine transcarbamoylase (EC 2.1.3.3) and urea levels in mice. The urea level was found elevated in liver, brain and plasma during P. yoelii infection. However, carbamoyl phosphate synthetase and ornithine transcarbamoylase were noticeably decreased during P. yoelii infection. Pyrimethamine treatment (10 mg/kg body weight for 4 days) brought back the altered parameters to normal a week after cessation of drug treatment.

Status of ammonia, glutamate, lactate and pyruvate during Plasmodium yoelii infection and pyrimethamine treatment in mice.

Ammonia, lactate, glutamate and pyruvate levels in blood, liver, brain, spleen and kidney were determined during Plasmodium yoelii infection and pyrimethamine treatment in mice. Ammonia and lactate levels showed significant increase with rise in parasitaemia except in spleen where decrease in the lactate levels was observed. The glutamate level displayed a marked decrease in blood, liver and splenic tissues, whereas, significant increase in glutamate level in kidney was observed, although its level in cerebral tissue remained unaltered. The pyruvate level in blood and liver showed a noticeable decrease but brain, spleen and kidney registered an elevation of the same due to the parasitic infection. Pyrimethamine (oral) treatment (10 mg/kg body weight) to infected mice (5-10%) for four days brought back the altered levels of the above cellular constituents in different tissues to normal, a week after cessation of drug treatment.

Effect of sodium stibogluconate on hepatic mixed function oxidase system and marker enzymes of golden hamsters during Leishmania donovani infection.

During L. donovani infection in golden hamsters, tremendous hepatic damage was observed as apparent from increased activities of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, succinate dehydrogenase, glucose-6-phosphatase and acid ribonuclease. The levels of cytochrome P-450 and related monooxygenases, viz. aniline hydroxylase and aminopyrine-N-demethylase registered significant decrease in infected animals. Sodium stibogluconate, a standard antileishmanial drug, though caused the removal of parasites from infected tissues, but did not help in the recovery of deranged hepatic markers. The results explain the higher mortality of stibanate treated infected animals as compared to untreated animals infected with L. donovani.

Hydrolytic enzymes of rhesus placenta during Plasmodium cynomolgi infection: ultrastructural and biochemical studies.

Placenta in monkey demonstrated altered pathophysiology after P cynomolgi infection. The electronmicroscopic observations showed slight complete focal necrosis of the placental tissue, besides alterations in total protein, phosphatases and proteinases. These changes in cellular constituents of placenta during malaria infection may be responsible for malfunctioning of the organ and in turn, abnormal development of foetus.

Partial purification of acid phosphomonoesterase in axenically grown Entamoeba histolytica NIH-200.

Entamoeba histolytica possesses significant acid phosphatase activity as compared to alkaline phosphatase activity. The acid phosphatase activity in the amoebic cells eluted at higher saline concentration as three distinct peaks at 200, 300 and 400 mM sodium chloride.

Specific features of phosphomonoesterase of Entamoeba histolytica (NIH-200).

Axenically grown E. histolytica possess significant acid phosphatase activity. The Km of the enzyme was found to be 7.1 x 10(-3) and was maximally active at pH 4.5. Acid phosphatase activity was significantly inhibited by Cu2+, cysteine and was activated by tartrate and fluoride. It was found that E. histolytica acid phosphatase differs in some properties as compared to the enzyme reported from other sources.

Effect of a new 8-aminoquinoline antimalarial compound on hepatic microsomal mixed function oxidase system of mice.

A new 8-aminoquinoline derivative (compound 80/53) synthesized at the Central Drug Research Institute, Lucknow (India), has been found to be an active anti-relapse (tissue schizontocidal) compound. Compound 80/53 at 8.75 mg/kg x 4 days and primaquine at 7.00 mg/kg (base) x 4 days given orally to Swiss mice led to inhibition of the different components of the hepatic microsomal mixed function oxidase system to varying degrees. Compound 80/53 inhibited cytochrome P-450, aminopyrine-N-demethylase, aniline and benzo (a) pyrene hydroxylase, cytochrome b5 and heme content of the normal mice by 12, 14, 0, 57, 20 and 6 per cent respectively, whereas the inhibition caused by primaquine in these components was 25, 21, 17, 48, 26 and 6 per cent respectively. Thus, there was less inhibition of hepatic microsomal MFO system of mice by compound 80/53 as compared to that by primaquine.