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Biomedical subjects

Q Rahman

Publications and source records attributed to Q Rahman.

At least 55 records · Page 3Linked to original sources
PubMed1990

Effect of chrysotile asbestos on cytochrome P-450-dependent monooxygenase and glutathione-S-transferase activities in rat lung.

The in vitro and in vivo effect of a carcinogenic variety of asbestos, chrysotile, both on xenobiotic metabolizing enzymes such as benzo[a]pyrene hydroxylase, epoxide hydrolase as well as glutathione-S-transferase activities and microsomal lipid peroxidation in rat lung were examined. The in vitro incubation of chrysotile with microsomes significantly adsorbed heme proteins, cytochrome P-450 and P-448 with the concomitant decrease in the dependent monooxygenase activities. The prolonged incubation of this mineral fibre with microsomes also resulted in the release of heme. It also led to the depletion in the activities of epoxide hydrolase and glutathione-S-transferase. However, it induced lipid peroxidation. When these in vitro effects were validated in vivo, the exposure to early stages produced similar alterations as observed in in vitro studies. However, reverse pattern in the alterations was observed after 90 days of exposure except in the case of lipid peroxidation which remained induced.

Adsorption↗
PubMed1990

Protective role of ascorbic acid against asbestos induced toxicity in rat lung: in vitro study.

Asbestos fibers adsorb cytochrome P-450 and P-448 proteins from rat lung micosomal fractions and liberate heme from cytochrome P-448 on prolonged incubation in vitro. further, fibers, decrease the activities of benzo(a)pyrene hydroxylase and glutathione-S-transferase in microsomal and cytosolic fractions respectively. Mineral fibers also stimulate both the enzymatic (NADPH-induced) and non-enzymatic (Fe2(+)-induced) lipid peroxidation in microsomal fractions. Preincubation of microsomal and cytosolic fractions with a physiological concentration of ascorbic acid ameliorates, to a large extent, the changes induced by asbestos fibers.

Animals↗
PubMed1989

Bioreactivity of intratracheally administered slate dust in rats: incorporation of 14C-acetate into lung lipids.

The effect of intratracheally instilled slate dust on the phospholipid profile, and 14C-acetate incorporation into the lipids of lung lavage, whole lung tissue and its subcellular fractions, has been studied in rats. The acellular fraction of lung lavage showed a decrease in the phospholipid content at 4 days and then an increase at 40 days of dust exposure, whereas the cellular fraction showed the reverse. The order of 14C-acetate incorporation into total lipids and individual phospholipids showed a parallel trend. The rate of incorporation with total lipids of lung tissue was higher at the two stages of dust exposure and a similar pattern prevailed in the subcellular fractions, i.e. mitochondrial, microsomal and cytosolic fraction. Acetate incorporation was highest in mitochondria, followed by the microsomes. An increase in the microsomal and mitochondrial cholesterol levels was also observed. There was no significant change in the solvent-extracted 14C-counts of whole plasma, trichloroacetic acid (TCA) precipitate and TCA supernatant of plasma. The results indicate that slate dust causes an enhanced synthesis of pulmonary surfactant and other lung lipids and, therefore, has an effect on the metabolism of type II alveolar epithelial cells.

Acetates↗
PubMed1988

Postmortem stability of somatostatin in brain tissue.

The stability of somatostatin (SS) in brain tissue was studied in human material obtained post-mortem and in the rat. In both human and rat brain, loss of SS was found to occur in tissue frozen to -70 degrees C. In the rat, this loss varied from 26 to 70 percent depending on the type of tissue processing used. These data suggest that, for the study of SS in post-mortem brain, use of frozen material should be avoided.

Adult↗
PubMed1988

Strand breakage in DNA by silicic acid.

The alkaline unwinding assay has been used to demonstrate the formation of single-strand breaks in DNA on treatment with silicic acid. Double-stranded DNA, containing no single-strand breaks, when incubated with increasing concentrations of silicic acid, showed the formation of an increasing number of strand breaks per molecule. Experiments on reduction of silicic acid-treated DNA with NaBH4 suggested the possibility of creation of apurinic or apyrimidinic sites. The significance of silicic acid interaction with cellular DNA during asbestos exposure is discussed.

Borohydrides↗
PubMed1987

Interrelationship between hemolysis and lipid peroxidation of human erythrocytes induced by silicic acid and silicate dusts.

Silicic acid and silicate dusts (slate dust and chrysotile asbestos) cause hemolysis of erythrocytes in vitro. The peroxidation of polyunsaturated fatty acids (PUFA) of erythrocyte membrane lipids is also enhanced by incubating the erythrocytes with silicic acid and silicate dusts in in vitro. Hemolysis of erythrocytes elicited by silicic acid and silicate dusts is inhibited significantly by polyvinyl-pyrrolidone and dipalmitoyl lecithin (DPL). These agents, however, have no effect on silicic acid and silicate dust induced peroxidation of erythrocyte membrane lipids. On the other hand, peroxidation of erythrocyte membrane lipids, induced by silicic acid and silicate dusts, is inhibited almost completely by adding superoxide dismutase and catalase to the incubation system, whilst the hemolysis of erythrocytes induced by silicic acid and silicate dusts is unaffected by these agents. Similarly the lysis of erythrocytes, induced by silicic acid and silicate dusts, proceeds at a much faster rate than silicic acid and silicate dust induced lipid peroxidation. These results indicate that silicic acid and silicate dust induced hemolysis and lipid peroxidation represent two independent processes.

Asbestos↗
PubMed1985

Interaction of silica with plasma proteins: in vivo studies.

Silicic acid has been shown to be the main pathogenic factor in the toxicity of silicate dusts. Our earlier findings have shown the interaction of silica (silicic acid) with rat plasma and lung proteins in vitro. In the present communication, we report the binding of silica with plasma protein in vivo. The significance of in vivo silica-protein interaction is discussed in relation to its toxicity and clearance from the body.

Animals↗
PubMed1985

Effect of slate dust on the rat erythrocyte membrane composition: in vitro and in vivo studies.

The biochemical composition of rat erythrocyte ghost membrane obtained by hypotonic lysis and slate-dust-induced lysis were compared in vitro. The phospholipids and glycosamine contents decreased in slate-dust-exposed erythrocyte membrane, whereas there were no changes in protein content. The in vitro and in vivo association of silica, leaching from slate dust, with the components of rat erythrocyte ghost membrane, has also been demonstrated. The interaction of silica with membrane constituents is proposed as a mechanism of action of slate-dust toxicity.

Amino Sugars↗
PubMed1984

Pulmonary biochemical response to slate dust in rats.

The biochemical changes in rat lungs due to intratracheal instillation of 50 mg of slate dust have been studied up to 150 days of dust exposure. The remarkable feature of lung changes was the turnover of collagen in experimental animals after 90 days, reaching substantially higher values at 150 days. A concurrent increase in hexosamine and sialic acid contents was also observed. The phospholipid content in the whole lung tissue, as well as in the mitochondria, was generally higher in the dust-treated rats, particularly at the later stages. The mitochondrial cytochrome c oxidase and glutamate dehydrogenase activities increased, whereas monoamine oxidase was marginally affected. Mitochondria from experimental animals appeared to be in a swollen state, particularly at 120 days of exposure. The above results suggest that slate dust exerts its toxic effects by causing alterations in the tissue make-up as well as in the mitochondrial functioning of the lung.

Animals↗
PubMed1984

Interaction of silicate dust with erythrocyte ghost membrane: in vitro studies.

Composition of the erythrocyte ghost membrane obtained from slate-dust-lysed and hypotonically lysed erythrocytes were compared in vitro. The protein and cholesterol contents were unaltered, whilst phospholipid and glycosamine contents decreased significantly in the slate-dust-lysed preparation of erythrocyte ghost membrane. Na+, K+-ATPase activity remained unchanged, whilst acetylcholinesterase activity was decreased slightly by slate dust treatment. Further, binding of silicic acid, dissolving out of slate dust, was observed with a component of erythrocyte ghost membrane protein having molecular weight around 90 000 daltons. The significance of the findings is discussed.

Carrier Proteins↗
PubMed1984

The binding of silica to proteins from plasma and lungs of rat: in vitro.

Silica dissolving out from the slate dust was found to bind with plasma protein and purified bovine serum albumin. At 24 h of incubation at 37 degrees C binding affinity of silica (microgram of silica bound/mg of protein) with plasma protein and bovine serum albumin was found to be 0.59 and 0.44, respectively. By molecular exclusion chromatography using Sephadex G-200, silica binding protein of plasma was determined to be of mol. wt. around 67000. Similar proteins having silica binding capacity (mol. wt. 70000 and 85000) were also found in rat lung but these proteins unlike their plasma counterpart were glycoprotein in nature. Polyacrylamide gel electrophoresis of plasma and protein rich lung fraction show that proteins upon binding with silica undergo mobility changes. Significance of the existence of silica binding protein in plasma and lung of rat in relation to silica toxicity is discussed.

Animals↗
PubMed1984

Degradation of DNA by silicic acid.

S1 nuclease hydrolysis and hydroxyapatite chromatography were used to study the effect of silicic acid on DNA. Native calf thymus DNA was incubated with increasing concentrations of silicic acid (DNA nucleotide/silicic acid molar ratios of 1:0.25, 1:0.5 and 1:1) and subjected to S1 nuclease hydrolysis. An increasing degree of DNA degradation was seen suggesting a destabilization of the secondary structure. A decrease in melting temperature was also observed. Hydroxyapatite chromatography indicated that incubation at the molar ratio of 1:1 resulted in denaturation and degradation of DNA.

Animals↗
PubMed1983

Relationship between solubility and hemolytic effects of toxic dusts.

Two varieties of native and chemically treated slate dust were tested in vitro for their hemolytic effects and the extent of silicic acid dissolution in various physiological fluids. The extent of hemolysis was found to be proportional to the degree of dissolution of dust constituents. Membrane lysis by the dust appeared to be prevented by coating it with polyvinyl pyrrolidone, serum proteins and pulmonary lavage lipids. The significance of the findings is discussed.

Animals↗
PubMed1983

Binding of silicic acid by proteins and its relation to toxicity of silicate dusts.

A possible mechanism of biological effects of silicate dusts is the interaction between silicic acid and tissue constituents, and this has been studied in vitro. On incubating silicic acid with lung homogenate, appreciable amounts of silicon were recovered in the trichloroacetic acid precipitate in both organic solvent extract and residual protein. Polyvinyl pyrrolidone inhibited this interaction as well as reducing the dissolution of silicic acid from asbestos dust. The capacity of serum albumin to bind silicic acid was also observed. Chemical interaction between macromolecules and silicic acid could be one of the factors responsible for the biological effects of silicon-containing dusts.

Animals↗
PubMed1983

Lung mitochondria in experimental asbestosis.

Alterations in lung mitochondria were followed in guinea pigs at different periods after a single intratracheal injection of chrysotile dust. Cytochrome c oxidase and succinic dehydrogenase activities showed gradual increase after 90 days, whereas monoamine oxidase remained unaffected throughout the study. There was an increase in glutamate dehydrogenase activity in postmitochondrial as well as in mitochondrial fractions, the latter being accompanied by decreased latency of the enzyme. Mitochondria from asbestotic lung appeared to be more swollen than in normal animals at and after 90 days of exposure. There were fluctuations in the contents of different phospholipids as a result of asbestosis. Beyond 90 days, collagen and mucopolysaccharides also increased. The results confirm the contention that pulmonary mitochondria are among the major target sites in asbestosis.

Animals↗
PubMed1983

Biochemical studies on the toxicity of hematite dust.

Biochemical alterations in guinea pig lungs caused by hematite dust were followed at 150 days after intratracheal administration of the dust. In vivo dust exposure caused a significant increase in mitochondrial protein content and cytochrome c oxidase activity whereas diaphorase activity remained unaltered. Mitochondria from the exposed animals were apparently in a swollen state and their contraction profile upon the addition of ATP reflected permeability changes. However, in vitro dust caused no significant alterations. Significant increases in glycogen content along with an insignificant decrease in glycogen phosphorylase activity were also observed in hematite-treated guinea pig lungs. Decrease in drug-metabolizing enzymes such as aniline hydroxylase and tyrosine aminotransferase activities were also evident in the postmitochondrial fraction of the siderotic lungs. [3H]Leucine-incorporation studies showed increased protein synthesis in the postmitochondrial fraction. Increase in protein synthesis in mitochondria was only marginal whereas in whole homogenate it decreased considerably. Experiments employing dust tagged with radioactive iron indicated the rapid mobilization of iron from lung and its distribution to various organs. The presence of iron-binding protein was confirmed by employing Sephadex gel-filtration techniques.

Animals↗
PubMed1983

Adsorption of nucleic acids on asbestos fibers in vitro.

Adsorption of DNA and RNA, accompanied by liberation of orthophosphate, occurred on contact with chrysotile asbestos fibers. This indicated that interaction of macromolecules and their components may be a factor, possibly involved in the manifestation of the toxic effect of asbestos fibers.

Adsorption↗