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Biomedical subjects

C K Pushpendran

Publications and source records attributed to C K Pushpendran.

At least 19 recordsLinked to original sources
PubMed1998

Study on lipid peroxidation potential in different tissues induced by ascorbate-Fe2+: possible factors involved in their differential susceptibility.

Susceptibility of four major rat tissues to oxidative damage in terms of lipid peroxidation induced by in vitro by ascorbate-Fe2+ in homogenates and mitochondria has been examined. Lipid peroxidation, as assessed by thiobarbituric acid reactive substances (TBARS) and conjugated dienes was maximum in brain followed by liver, kidney and heart. However, the time course of lipid peroxidation showed different patterns in tissues examined. The higher susceptibilities of brain and liver can be explained by substrate availability and to a lesser extent the level of antioxidants. The differences observed in the tissues studied may reflect their susceptibility to degenerative diseases and xenobiotic toxicity which are considered as a result of oxidative damage to membranes.

Animals↗
PubMed1994

Developmental changes in the peroxidation potential of rat brain homogenate and mitochondria.

Lipid peroxidation, one of the most common expressions of oxidative stress, may be altered during normal physiological states including development. We have examined the changes in lipid peroxidation in rat brain, a tissue highly susceptible to oxidative damage, during this physiological state. In vivo lipid peroxidation was moderate in the foetal and neonatal period and increased during the postnatal development. Lipid peroxidation potential in brain homogenate and mitochondria, in Tris-HCl buffer or with exogenous cofactors, such as ascorbate-Fe2+, NADPH ADP-Fe3+ and cumene hydroperoxide, showed significant changes during pre- and postnatal development. In general, brain as well as liver (used as a standard tissue for comparison) seem to have low peroxidation potential in the foetal and neonatal period which then increases at different rates during development to reach adult values at different days. The low peroxidation potential corresponds to the rapid phase of cell proliferation. These results taken together with similar earlier finding in other systems may indicate a possible occurrence of a 'permissible period' during which the low levels of lipid peroxidation may be able to yield only low amounts of cytostatic aldehydes and peroxides as byproducts, thereby allowing rapid proliferation of cells.

Animals↗
PubMed1986

Activation of phospholipase A2 by carbon tetrachloride in isolated rat hepatocytes.

Freshly isolated rat hepatocytes were exposed to carbon tetrachloride (CCl4) for periods up to 4 hr. Phospholipase A2 activity of these preparations was determined by measuring either the release of [3H]arachidonic acid from cellular phospholipids prelabeled with [3H]arachidonic acid or by measuring the formation of [14C]lysophosphatidylethanolamine from cellular lipids prelabeled with [14C]ethanolamine. Through the use of hexane-partition extraction and thin-layer chromatographic analysis of hepatocyte lipid extracts it was found that CCl4 stimulated phospholipase A2 activity in a dose- and time-dependent manner. Carbon tetrachloride at concentrations of 0.23 to 1.3 mM produced a 1.4- to 5.3-fold increase in phospholipase activity which was initiated within 30-60 min of incubation at 37 degrees. The role of phospholipase activation as a secondary mechanism of CCl4-induced hepatocyte injury is discussed.

Animals↗
PubMed1986

Changes in ascorbate-induced lipid peroxidation of hepatic rough and smooth microsomes during postnatal development and ageing of rats.

In female Wistar rats, sensitivity to ascorbate-induced lipid peroxidation in rough and smooth microsomes increases with age, reaching a maximum in 1-year-old rats and decreases during ageing. Time course of lipid peroxidation, and lipid peroxidation with optimum concentrations of ascorbic acid, Fe2+ and protein in rough microsomes show that 1-year-old rats are the most susceptible followed by 75-day-old, 15-day-old, 2-year-old and 1-day-old rats. However, smooth microsomes show a slightly different trend with maximum sensitivity in 1-year-old rats followed by 15-day-old, 75-day-old, 2-year-old and 1-day-old rats. Smooth microsomes are more susceptible to lipid peroxidation than the rough in all age groups except 75-day-old rats. Smooth microsomes are also more sensitive to inhibitors of lipid peroxidation. Microsomal content of phospholipid increases during postnatal development and decreases during ageing, whereas that of ascorbic acid and alpha-tocopherol do not show any particular trend.

Aging↗
PubMed1985

Kinetics of NADPH-induced lipid peroxidation in rat liver microsomal fractions as a function of age.

The kinetics of NADPH-induced lipid peroxidation in hepatic rough and smooth microsomes have been studied in rats ranging in age from 1 day to 2 years. Apparent Km and Vmax for NADPH and the extent of lipid peroxidation show that lipid peroxidation potential is low at birth, increases during postnatal development, and decreases during senescence. Our results indicate that this trend may be due to changes in phospholipid content and NADPH cytochrome c reductase activity in microsomal fractions.

Aging↗
PubMed1984

RX781094 a potent and selective alpha 2-adrenergic antagonist. Effects in adipocytes and hepatocytes.

The potency and selectivity of RX781094, 2-(2-(1,4-benzodioxanyl]-2-imidazoline HCl, as alpha 1- and alpha 2-adrenergic antagonist was studied using rat hepatocytes and hamster adipocytes. The alpha 1-adrenergic stimulation of ureogenesis produced by epinephrine in rat hepatocytes was slightly diminished by 10(-4) M RX781094. On the contrary the alpha 2-adrenergic effect of epinephrine in hamster adipocytes (inhibition of adenylate cyclase) was antagonized dose-dependently by RX781094. This agent was approximately 10-fold more potent than yohimbine. Radioligand binding studies also showed that RX781094 was more potent and selective than yohimbine at alpha 2-adrenergic sites. It is concluded that RX781094 is a potent and selective alpha 2-adrenergic antagonist.

Adipose Tissue↗
PubMed1984

Effect of insulin on alpha1-adrenergic actions in hepatocytes from euthyroid and hypothyroid rats. Possible involvement of two pathways in alpha1-adrenergic actions.

The effect of insulin on the alpha1-adrenergic stimulation of glycogenolysis and ureogenesis, which is very small or undetectable in hepatocytes from control animals, is marked in hepatocytes from hypothyroid rats; the metabolic actions due to alpha1-adrenergic activation, but not those due to glucagon, were nearly blocked by insulin in cells from hypothyroid rats. The alpha1-adrenergic-mediated stimulation of phosphatidylinositol labelling was not affected by insulin in cells from either control or hypothyroid rats. The data suggest that the alpha1-adrenergic action proceeds through two pathways, one of which is very sensitive to insulin and predominates in cells from hypothyroid rats.

Animals↗
PubMed1983

Effect of pertussis toxin on hormonal responsiveness of rat hepatocytes.

The ureogenic action of epinephrine in hepatocytes from normal adult rats is mediated through activation of alpha 1-adrenoceptors. beta-Adrenoceptors in addition to alpha 1-adrenoceptors, became involved in mediating this effect in cells from animals treated with pertussis toxin. The accumulation of cyclic-AMP in response to epinephrine or isoproterenol was markedly increased in hepatocytes from pertussis-treated rats as compared to that observed in control cells. The accumulation of cyclic-AMP due to glucagon was also increased. It is suggested that pertussis toxin may release a constraint on adenylate cyclase activity by blocking the inhibitory coupling mechanism (Ni) or some other entity involved in the regulation of the activity of this enzyme.

Adenylate Cyclase Toxin↗
PubMed1983

Differences in lipid peroxidation of rat liver rough and smooth microsomes.

The rough and smooth microsomes of rat liver show significant differences in lipid peroxidation induced by both NADPH and ascorbate. The parameters studied include kinetics, response towards cofactors and sensitivity to inhibitors. Smooth microsomes are more prone to lipid peroxidation with increasing concentrations of NADPH, Fe3+, ascorbate and Fe2+, and are more susceptible to inhibitors than rough microsomes. Smooth microsomes also contain higher amounts of ascorbic acid, NADPH cytochrome c reductase and total lipids, besides possessing a higher degree of unsaturation in lipids, all of which promote lipid peroxidation. Our results suggest that, although smooth microsomes are more sensitive to lipid peroxidation, they are compensated for by being more sensitive to inhibitors of lipid peroxidation.

Animals↗
PubMed1983

Age-related effect of cycloheximide on lipid peroxidation in rough and smooth microsomes of rat liver.

Cycloheximide, at a nonlethal dose of 2 mg/kg body weight, has different effects on microsomal in vivo lipid peroxidation in different age groups. In general, the antibiotic increases microsomal lipid peroxidation in newborn and 1-year-old rats, but decreases it in 15- and 75-day-old rats. Low doses of cycloheximide induces lipid peroxidation in vitro whereas higher doses cause inhibition. The degree of change differs in the two microsomal fractions. The sucklings are more susceptible to such a change than the older rats. In vivo lipid peroxidation in rat liver homogenate and rough and smooth microsomes declines as a function of age. Smooth microsomes show more lipid peroxidation than the rough in the different age groups.

Aging↗
PubMed1982

Effect of cycloheximide on hepatic microsomal lipids as a function of age in rats.

Cycloheximide, at a non-lethal dose of 2 mg/kg body weight, increases the level of total lipids and major lipid fractions in total, rough and smooth liver microsomes obtained from suckling, adult and old rats, but not in the newborns. The rates of increase differ in the different age-groups and fractions. Total lipids and phosphatidyl choline of rough and smooth microsomes in adult rats reach control levels at 6 h after the antibiotic treatment. Phospholipid fractions of old rats tend to approach control levels by 6 h after treatment whereas cholesterol levels remain relatively high. Total lipids, phosphatidyl choline and phosphatidyl ethanolamine of total, rough and smooth microsomes show significant quantitative differences during development.

Aging↗
PubMed1980

The metabolic fate of [35S]-diallyl disulphide in mice.

Diallyl disulphide (DADS) is a major constituent of garlic oil. Uptake of [35S]-labelled diallyl disulphide by mouse liver is highest at 90 min after treatment with [35S]-DADS, 70% of the radioactivity is present in the liver cytosol of which 80% is metabolized to sulphate.

Allyl Compounds↗