Biomedical subjects

M Bagchi

Publications and source records attributed to M Bagchi.

At least 55 records · Page 3Linked to original sources

PubMed1998

Naphthalene-induced oxidative stress and DNA damage in cultured macrophage J774A.1 cells.

Naphthalene is a bicyclic aromatic compound that is widely used in various domestic and commercial applications including lavatory scent disks, soil fumigants and moth balls. However, little information is available regarding the mechanism of naphthalene toxicity. We have assessed the concentration-dependent in vitro effects of naphthalene on increased lipid peroxidation, cytochrome c reduction, hydroxyl radical production, modulation of intracellular oxidized states by laser scanning confocal microscopy, and DNA fragmentation in cultured macrophage J774A.1 cells. The cells were incubated with 0-500 microM concentrations of naphthalene for 0, 12 and 24 h at 37 degrees C. Concentration- and time-dependent changes were observed. No significant changes were observed with concentrations of naphthalene up to 100 microM. At 24 h, lipid peroxidation increased by 1.8-, 2.4- and 2.9-fold at 200, 300 and 500 microM concentrations of naphthalene. Approximately 2.0-, 3.1- and 4.6-fold increases in cytochrome c reduction were observed at 200, 300 and 500 microM concentrations of naphthalene, respectively, at this time point demonstrating the production of superoxide anion, while under the same conditions approximately 2.4-, 3.2- and 4.9-fold increases in hydroxyl radical production were observed, respectively. Following incubation of these cells with 200 and 500 microM concentrations of naphthalene 2.3- and 4.7-fold increases in fluorescence intensity were observed, respectively, as compared to the untreated cells. At 24 h, approximately 1.8-, 2.3- and 3.0-fold increases in DNA fragmentation were observed following incubation with 200, 300 and 500 microM concentrations of naphthalene, respectively. Naphthalene also produced concentration- dependent decreases in cell viability. At the 12 h time point, significant changes were observed only with 300 and 500 microM concentrations of naphthalene. These results demonstrate that naphthalene may induce toxic manifestations by enhanced production of oxygen free radicals, resulting in lipid peroxidation and DNA damage.

Animals↗

PubMed1998

Subchronic effects of smokeless tobacco extract (STE) on hepatic lipid peroxidation, DNA damage and excretion of urinary metabolites in rats.

The oral use of moist smokeless tobacco products (snuff) is causally associated with cancer of the mouth, lip, nasal cavities, esophagus and gut. The mechanism by which smokeless tobacco constituents produce genetic and tissue damage is not known. Recent studies in our laboratories have shown that an aqueous extract of smokeless tobacco (STE) activates macrophages with the resultant production of reactive oxygen species (ROS), including nitric oxide. Furthermore, the administration of acute doses of STE (125-500 mg/kg) to rats induces dose dependent increases in mitochondrial and microsomal lipid peroxidation, enhances DNA single strand breaks, and significantly increases the urinary excretion of the lipid metabolites malondialdehyde, formaldehyde, acetaldehyde and acetone. Since the use of tobacco is a chronic process, the effects of an aqueous extract of STE in rats following low dose exposure were examined. Female Sprague-Dawley rats were treated orally with 25 mg STE/kg every other day for 105 days. The effects of subchronic treatment of STE on hepatic microsomal and mitochondrial lipid peroxidation and the incidence of hepatic nuclear DNA damage were assessed. Lipid peroxidation increased 1.4- to 3.3-fold in hepatic mitochondria and microsome with STE treatment between 0 and 105 days with respect to control animals while hepatic DNA single strand breaks increased up to 3.4-fold. Maximum increases in lipid peroxidation and DNA single strand breaks occurred between 75 and 90 days of treatment. Urinary excretion of the four lipid metabolites malondialdehyde, formaldehyde, acetaldehyde and acetone was monitored by high pressure liquid chromatography (HPLC) with maximum increases being observed between 60 and 75 days of treatment. The results clearly indicate that low dose subchronic administration of STE induces an oxidative stress resulting in tissue damaging effects which may contribute to the toxicity and carcinogenicity of STE.

Acetaldehyde↗

PubMed1998

Protective effects of zinc salts on TPA-induced hepatic and brain lipid peroxidation, glutathione depletion, DNA damage and peritoneal macrophage activation in mice.

1. The comparative protective abilities of zinc L-methionine, zinc DL-methionine, zinc sulfate, zinc gluconate, L-methionine, DL-methionine, and vitamin E succinate (VES) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced lipid peroxidation, DNA fragmentation, and glutathione depletion in the hepatic and brain tissues, and production of reactive oxygen species by peritoneal macrophages were assessed. In addition, mice were fed a zinc-deficient diet for 5 weeks, and treated with TPA and/or zinc L-methionine or zinc DL-methionine, and similar studies were conducted. 2. The zinc-deficient diet induced oxidative stress in the hepatic and brain tissues as well as in the peritoneal macrophages as evidenced by significantly enhanced lipid peroxidation. DNA fragmentation, glutathione depletion, and production of reactive oxygen species. 3. Treatment of mice with zinc L-methionine, zinc DL-methionine, and VES decreased TPA-induced reactive oxygen species production as evidenced by significant decreases in chemiluminescence in peritoneal macrophages by approximately 45%, 31%, and 47%, respectively, and cytochrome c reduction by approximately 54%, 35%, and 41%, respectively, as compared with control values. Similar results were observed with liver and brain lipid peroxidation, DNA fragmentation, and glutathione depletion. 4. Zinc salts and antioxidants provided significant protection against TPA-induced oxidative damage. Zinc L-methionine provided the best protection.

Animals↗

PubMed1998

Protective effects of grape seed proanthocyanidins and selected antioxidants against TPA-induced hepatic and brain lipid peroxidation and DNA fragmentation, and peritoneal macrophage activation in mice.

1. The comparative protective abilities of a grape seed proanthocyanidin extract (GSPE) (25-100 mg/kg), vitamin C (100 mg/kg), vitamin E succinate (VES) (100 mg/kg) and beta-carotene (50 mg/kg) on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced lipid peroxidation and DNA fragmentation in the hepatic and brain tissues, as well as production of reactive oxygen species by peritoneal macrophages, were assessed. 2. Treatment of mice with GSPE (100 mg/kg), vitamin C, VES and beta-carotene decreased TPA-induced production of reactive oxygen species, as evidenced by decreases in the chemiluminescence response in peritoneal macrophages by approximately 70%, 18%, 47% and 16%, respectively, and cytochrome c reduction by approximately 65%, 15%, 37% and 19%, respectively, compared with controls. 3. GSPE, vitamin C, VES and beta-carotene decreased TPA-induced DNA fragmentation by approximately 47%, 10%, 30% and 11%, respectively, in the hepatic tissues, and 50%, 14%, 31% and 11%, respectively, in the brain tissues, at the doses that were used. Similar results were observed with respect to lipid peroxidation in hepatic mitochondria and microsomes and in brain homogenates. 4. GSPE exhibited a dose-dependent inhibition of TPA-induced lipid peroxidation and DNA fragmentation in liver and brain, as well as a dose-dependent inhibition of TPA-induced reactive oxygen species production in peritoneal macrophages. 5. GSPE and other antioxidants provided significant protection against TPA-induced oxidative damage, with GSPE providing better protection than did other antioxidants at the doses that were employed.

Animals↗

PubMed1998

Nuclear matrix associated DNA-binding proteins of ocular lens epithelial cells.

Association of transcription factors with the nuclear matrix represents a mechanism by which nuclear architecture may influence transcriptional control of gene expression. This investigation examines nuclear matrix associated proteins (NMP's) isolated from ocular lens epithelial cells by monitoring DNA binding activities using consensus oligonucleotides recognized by the transcription factors YY1, AML-1, AP-1, SP-1 and ATF. The nuclear matrix fractions tested included an immortilized human lens epithelial cell line containing the SV40 large T-antigen, and two mouse lens epithelial cell lines derived from either a normal mouse or a cataract mouse. A rabbit epidermal epithelial cell line and HeLa cells were also included in this study for comparison. The data from these experiments reveal that ubiquitously represented and tissue restricted regulatory proteins are associated with nuclear matrix of lens epithelial cells. The functional significance of the nuclear matrix association of these transcription factors remains to be determined. However, our findings raise the possibility that the transcription factors associated with the nuclear matrix could have specific roles in gene regulation and eye tissue development.

Animals↗

PubMed1998

Induction of oxidative stress and DNA damage by chronic administration of naphthalene to rats.

Administration, Oral↗

PubMed1998

Protective ability of acetylsalicylic acid (aspirin) to scavenge radiation induced free radicals in J774A.1 macrophage cells.

Radiation generates a variety of free radicals during the exposure of biological tissues through radiolysis of water. These free radicals are highly reactive and cause oxidative damage to biological molecules. This study examined the protective ability of aspirin against radiation induced oxidative stress. The study assessed the protective effect of aspirin (0.05 mM, 0.10 mM, 0.50 mM) on the generation of free radicals during exposure of J774A.1 macrophage cells to radiation (13.25 cGy). Approximately a 2.2-fold increase in superoxide anion formation as determined by cytochrome c reduction was observed following exposure of the cells to radiation for 20 one second exposures. Preincubation with aspirin exhibited a dose dependent decrease in free radical production as assessed by chemiluminescence and cytochrome c reduction. Aspirin also produced a concentration dependent reduction in radiation induced DNA damage in the cells. The data indicate that radiation of these cells results in production of reactive oxygen species and DNA damage, and aspirin can decrease these effects in a concentration dependent manner.

Analysis of Variance↗

PubMed1997

Interrelationship between cellular calcium homeostasis and free radical generation in myocardial reperfusion injury.

This review describes the interrelationship between two important biological factors, intracellular calcium overloading and oxygen-derived free radicals, which play a crucial role in the pathogenesis of myocardial ischemic reperfusion injury. Free radicals are generated during the reperfusion of ischemic myocardium, and polyunsaturated fatty acids in the membrane phospholipids are the likely targets of the free radical attack. On the other hand, activation of phospholipases can provoke the breakdown of membrane phospholipids which results in the activation of arachidonate cascade leading to the generation of prostaglandins, and oxygen free radicals can be produced during the interconversion of the prostaglandins. In conclusion, it has been emphasized that the two seemingly different causative factors of reperfusion injury, intracellular calcium overloading and free radical generation are, in fact, highly interrelated.

Calcium↗

PubMed1997

Nonchromatin nuclear proteins of mammalian lens epithelial cells.

The nuclear matrix (NM) proteins of six tissue cultured lens epithelial cell lines and one embryonic rabbit epidermal cell line were analyzed to determined possible tissue and species specificity of these proteins. The NM proteins were isolated by the modified Penman technique. The tissue cultured cells were pulsed with [35S] methionine and nuclear matrix proteins were fractionated by two-dimensional (2-D) gel electrophoresis. The 2-D gels were dried and autoradiographed. The relative abundance of spot patterns of nuclear matrix proteins of different cells were compared. The data from these experiments revealed that all the examined cell lines have distinct spot patterns, however, all of NM profile showed a spot pattern in the 45 kDa region with acidic pH. Some of these spots cross-reacted with anti-vimentin antibodies, whereas a prominent protein spot in this region did not cross react with either vimentin or actin antibodies. The observed variations in the NM protein patterns of lens epithelial cells may reflect tissue and species specificity and also a role in the regulatory properties of these nuclear proteins in the eye tissue development.

Animals↗

PubMed1997

Comparative in vitro and in vivo protein kinase C activation by selected pesticides and transition metal salts.

Various pesticides and transition metals induce oxidative deterioration of biological macromolecules. Protein kinase C (PKC) may mediate these effects. However, no information is available regarding whether these xenobiotics can modulate PKC which is a critical event signaling the increase in endothelial permeability and cell proliferation. Female Sprague-Dawley rats were treated p.o. with two 0.25 LD50 doses of selected pesticides and transition metal salts at 0 and 21 h, and killed at 24 h. PKC activities were measured in liver and brain tissues. Cultured PC-12 cells were incubated for 24 h with 50, 100 or 200 nM concentrations of these pesticides, while 0.20, 0.40 or 0.60 microM concentrations of cadmium chloride (Cd(II)) and sodium dichromate (Cr(VI)) salts were employed. PKC activations were observed in the hepatic and brain cytosol fractions by all xenobiotics. Approximately 1.4- to 2.0-fold and 1.6- to 3.5-fold increases in PKC activity in the hepatic and brain cytosol fractions were observed, respectively. In the hepatic tissues, the greatest increases in activities were observed with TCDD, chlorpyrifos, endrin and Cd(II), while chlorpyrifos and fenthion exerted the greatest increases in the brain tissues. In cultured PC-12 cells, the greatest activation of PKC was observed primarily with 100-nM concentrations of the pesticides. The maximum effects were induced by chlorpyrifos, fenthion, Cd(II) and Cr(VI) salt. The results clearly indicate that pesticides as well as Cd(II) and Cr(VI) salts can modulate a vital component of the cell signaling pathway, namely PKC activity. PKC may be a target of free radicals and oxidative stress, leading to altered cell proliferation and differentiation.

Animals↗

PubMed1997

Comparative in vitro oxygen radical scavenging ability of zinc methionine and selected zinc salts and antioxidants.

1. The concentration-dependent scavenging abilities of zinc DL-methionine, zinc sulfate, zinc gluconate, zinc picolinate and selected free radical scavengers, including superoxide dismutase (SOD), catalase, mannitol, allopurinol and DL-methionine, were examined against biochemically generated superoxide anion, hydroxyl radical and hypochlorite radical plus hypochlorous acid, by chemiluminescence and cytochrome c reduction. 2. Zinc methionine was the most effective of the zinc compounds that were tested. Following incubations with superoxide anion, hydroxyl radical, and hypochlorite radical-generating systems, in the presence of 50 microM zinc DL-methionine approximately 38%, 47% and 28% inhibition in reactive oxygen species generation was observed, respectively, compared to control groups. 3. The protective abilities of various zinc salts, as well as selected free radical scavengers and antioxidants were also assessed on phorbol ester (TPA)-induced lactate dehydrogenase (LDH) release from cultured PC-12 cells. Preincubation showed better protection than coincubation. Approximately 45% and 50% inhibition in TPA-induced LDH leakage was observed following preincubation with 50 microM zinc DL-methionine and 50 microM vitamin E succinate, respectively. Zinc DL-methionine exhibited better protection against LDH leakage than any other zinc salt tested. 4. The results indicate that zinc DL-methionine can attenuate the biochemical consequences of oxygen free radicals, and is comparable to other well-known antioxidants and free radical scavengers in the in vitro system that was employed.

Animals↗

PubMed1997

Induction of oxidative stress by chronic administration of sodium dichromate [chromium VI] and cadmium chloride [cadmium II] to rats.

Recent studies have demonstrated that both chromium (VI) and cadmium (II) induce an oxidative stress, as determined by increased hepatic lipid peroxidation, hepatic glutathione depletion, hepatic nuclear DNA damage, and excretion of urinary lipid metabolites. However, whether chronic exposure to low levels of Cr(VI) and Cd(II) will produce an oxidative stress is not shown. The effects of oral, low (0.05 LD50) doses of sodium dichromate [Cr(VI); 2.5 mg/kg/d] and cadmium chloride [Cd(II); 4.4 mg/kg/d] in water on hepatic and brain mitochondrial and microsomal lipid peroxidation, excretion of urinary lipid metabolites including malondialdehyde, formaldehyde, acetaldehyde and acetone, and hepatic nuclear DNA-single strand breaks (SSB) were examined in female Sprague-Dawley rats over a period of 120 d. The animals were treated daily using an intragastric feeding needle. Maximum increases in hepatic and brain lipid peroxidation were observed between 60 and 75 d of treatment with both cations. Following Cr(VI) administration for 75 d, maximum increases in the urinary excretion of malondialdehyde, formaldehyde, acetaldehyde, and acetone were 2.1-, 1.8-, 2.1-, and 2.1-fold, respectively, while under the same conditions involving Cd(II) administration approximately 1.8-, 1.5-, 1.9-, and 1.5-fold increases were observed, respectively, as compared to control values. Following administration of Cr(VI) and Cd(II) for 75 d, approximately 2.4- and 3.8-fold increases in hepatic nuclear DNA-SSB were observed, respectively, while approximately 1.3- and 2.0-fold increases in brain nuclear DNA-SSB were observed, respectively. The results clearly indicate that low dose chronic administration of sodium dichromate and cadmium chloride induces an oxidative stress resulting in tissue damaging effects that may contribute to the toxicity and carcinogenicity of these two cations.

Acetaldehyde↗

PubMed1997

Protection against chemically-induced oxidative gastrointestinal tissue injury in rats by bismuth salts.

Oxygen free radicals (OFR) are implicated in the pathogenesis of stress, chemically induced gastric lesions, and gastrointestinal injury. The concentration-dependent scavenging abilities of bismuth subsalicylate (SBS), colloidal bismuth subcitrate (CBS), and selected OFR scavengers, including superoxide dismutase (SOD), catalase, mannitol, and allopurinol were examined against biochemically or chemically generated superoxide anion, hydroxyl radical, and hypochlorite radical plus hypochlorous acid based on a chemiluminescence assay. Furthermore, both gastric (GM) and intestinal mucosa (IM) were individually exposed in vitro to these free radical generating systems, and the concentration-dependent protective abilities of SBS and CBS against lipid peroxidation (LP) were compared with selected OFR scavengers. In addition, 24-hr fasted rats were orally treated with the necrotizing agents 0.6 M HCl, 0.2 M NaOH, 80% ethanol, and aspirin (200 mg/kg). The extent of tissue injury in the GM and IM was determined by assessing LP, DNA fragmentation, and membrane microviscosity. Dose- and time-dependent in vivo protective abilities of CBS (100 mg/kg) and SBS (15 mg/kg) were also assessed. Following incubations with superoxide anion and hydroxyl radical generating systems in the presence of 125 mg SBS/liter, approximately 47% and 61% inhibitions were observed in the chemiluminescence response, respectively, while 48% and 46% inhibitions were observed with 125 mg CBS/liter. SBS and CBS exerted similar abilities towards hypochlorite radical plus hypochlorous acid. Approx. 3.1- and 3.7-fold increases in LP were observed in the GM and IM of rats following oral administration of 0.6 M HCl. Pretreatment of the rats with SBS and CBS decreased 0.6 M HCl-induced LP in the GM by approx. 39% and 27%, respectively, with similar decreases in LP in the IM. SBS exhibited better protective abilities towards 0.6 M HCl and 0.2 m NaOH-induced GM and IM injury as compared to CBS. SBS and CBS provided similar protection towards 80% ethanol-induced gastric injury, while CBS exerted a superior protective ability towards aspirin-induced gastric injury. The results demonstrate that both SBS and CBS can scavenge reactive oxygen species and prevent tissue damage produced by OFR.

Animals↗

PubMed1997

Oxygen free radical scavenging abilities of vitamins C and E, and a grape seed proanthocyanidin extract in vitro.

Proanthocyanidins, a group of polyphenolic bioflavonoids, have been reported to exhibit a wide range of biological, pharmacological and chemoprotective properties against oxygen free radicals. We have assessed the concentration-dependent oxygen free radical scavenging abilities of a grape seed proanthocyanidin extract (GSPE), vitamin C and vitamin E succinate (VES) as well as superoxide dismutase, catalase and mannitol against biochemically generated superoxide anion and hydroxyl radical using a chemiluminescence assay and cytochrome c reduction. A concentration-dependent inhibition was demonstrated by GSPE. At a 100 mg/l concentration, GSPE exhibited 78-81% inhibition of superoxide anion and hydroxyl radical. Under similar conditions, vitamin C inhibited these two oxygen free radicals by approximately 12-19%, while VES inhibited the two radicals by 36-44%. The combination of superoxide dismutase and catalase inhibited superoxide anion by approximately 83%, while mannitol resulted in an 87% inhibition of hydroxyl radical. The results demonstrate that GSPE is a more potent scavenger of oxygen free radicals as compared to vitamin C and VES.

Anthocyanins↗

PubMed1997

Comparative induction of oxidative stress in cultured J774A.1 macrophage cells by chromium picolinate and chromium nicotinate.

The concentration-dependent effects of chromium picolinate and chromium nicotinate were assessed on the enhanced production of reactive oxygen species including superoxide anion and hydroxyl radicals, and lipid peroxidation and DNA fragmentation in cultured macrophage J774A.1 cells. The macrophage cells were incubated with 0-50 micrograms/ml [corrected] concentrations of these chromium (III) salts for 0 and 24 hrs at 37 degrees C. Concentration-dependent effects were observed. Lipid peroxidation increased by 1.3-1.5-fold following treatment of these cells with chromium picolinate while at these same concentrations of chromium nicotinate approximately 1.2-1.8-fold increases in lipid peroxidation were observed. Increases of 1.0-1.5-fold occurred in the production of superoxide anion as determined by cytochrome c reduction following treatment with chromium picolinate while with these same concentrations and conditions only 1.1-1.2-fold increases in cytochrome c reduction were observed following treatment with chromium nicotinate. Approximately 1.2-1.5-fold increases in hydroxyl radical production were observed following treatment of these macrophage cells with increasing concentrations of chromium picolinate and chromium nicotinate. Incubation of the cells with 30-50 micrograms/ml concentrations of chromium picolinate produced 1.2-1.6 fold increases in DNA fragmentation, while under these same conditions with chromium nicotinate 1.2-1.3-fold increases in DNA fragmentation occurred. No significant loss in cell viability was observed with either chromium salt. These results demonstrate that incubation of macrophage J774A.1 cells with these chromium salts induces low levels of oxidative stress as demonstrated by the biochemical assay techniques employed in this study.

Cells, Cultured↗

PubMed1997

AgNOR expression in CNS neoplasms.

Silver colloid staining of nucleolar organiser regions (AgNORs) is used for assessing the proliferative potential of tumours. The present study aimed at evaluating the AgNOR indices in normal and reactive CNS tissue, benign and malignant CNS neoplasms. The study group comprised of tissue from 22 controls and 100 cases (53 benign & 47 malignant neoplasms). The mean AgNOR index of controls was 0.95, benign neoplasms 1.25 and malignant neoplasms 2.12. A statistically significant difference was observed in controls and cases (p < 0.001) and between benign and malignant tumours (p = 0.002). Mean indices for low and high grade astrocytoma also significantly differed (p < 0.001). Using ROC curves cut off values were obtained for differentiation of neoplastic from non neoplastic (AgNOR index 1.10), benign from malignant (AgNOR index 1.75) and low grade (I & II) from anaplastic (Gr III & IV) Astrocytomas (AgNOR index 1.62). A spectrum of gradually increasing AgNOR indices from normal, reactive, benign to low and high grade malignancy indicates the usefulness of this simple technique as a proliferative marker.

Astrocytoma↗

PubMed1996

Age-related changes in lipid peroxidation and antioxidant defense in Fischer 344 rats.

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Aging↗

PubMed1996

Identification of a ubiquitin-like protein in the mammalian vitreous humor.

An 8 kDa ubiquitin-like peptide (ULP) was isolated by high performance liquid chromatography from the rabbit vitreous humor, and the N-terminal amino acid sequence of this peptide showed complete homology with ubiquitin. Western blot revealed the presence of free ULP in both the iris-ciliary (IC) complex and the aqueous humor extracts. In the IC complex, fluorescence and immunoelectron microscopy detected high concentrations of ULP in the posterior epithelial cells, suggesting this tissue as a possible source of ULP in the ocular fluids. Significantly, this is the first time that the presence of free ULP has been reported in mammalian extracellular fluids. Furthermore, we recently demonstrated that the 8 kDa fraction of vitreous humor containing ULP is a potent inhibitor of protein synthesis [Banerjee et al. (1992): J Cell Biochem 49:66-73]. These findings taken together suggest a novel biological role for ULP in the control of lens cell growth.

Amino Acid Sequence↗