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Biomedical subjects

M Z Hussain

Publications and source records attributed to M Z Hussain.

At least 19 recordsLinked to original sources
PubMed1992

Detection of interleukin-1 beta in human periapical lesions.

Interleukins are involved in modulating bone cell activity. Interleukin-1 (IL-1) has been shown to be potent stimuli of bone resorption in organ culture. This hormone-peptide is produced primarily by monocytes and macrophages. Diverse inflammatory cell types are clearly present in periapical lesions. The purpose of this study was to detect IL-1 beta activity in human periapical lesions. Eight human periapical lesions were examined for the presence of IL-1 beta. Pulp tissue of clinically impacted teeth were used as controls. Each specimen was quick-frozen and stored in liquid nitrogen. IL-1 beta activity was measured with, an IL-1 beta enzyme-linked immunosorbent assay that used monoclonal antibodies specific for IL-1 beta. Periapical samples exhibited significant activity of IL-1 beta (mean 604.4 +/- 563.0 pg/mg protein), whereas normal pulp had no activity. These results demonstrate that IL-1 beta is produced and released locally in inflammatory periapical lesions to mediate bone resorption.

Adult↗
PubMed1992

Clinical and light microscopic observations of gingivitis and early ligature-induced periodontitis in the cynomolgus monkey.

Clinical and histological observations were made on gingivitis and ligature-induced periodontitis in 4 adult female cynomolgus monkeys (Macaca fascicularis) to define the changes occurring in the early periodontitis lesion. Silk ligatures were tied around selected posterior teeth and replaced weekly for 4 weeks. The changes from gingivitis to periodontitis induced by ligation, and back to a state of clinical health after ligature removal, scaling and polishing, were characterized by Plaque Index, Gingival Index, probing pocket depth, attachment loss, and histologic evaluation. A mild, chronic marginal gingivitis was the normal finding in the gingiva of posterior teeth. The inflammatory infiltrate in the connective tissue contained primarily lymphocytes. Hygienic measures once a week reduced the amount of infiltrate and the epithelial proliferation, but did not eliminate it. Placement of silk ligatures rapidly changed the clinical picture to a moderate or severe gingivitis, which presented an almost bizarre response of sulcular and oral epithelium, with an increase in polymorphonuclear neutrophil infiltration. Within 2 weeks there was significant probing attachment loss. The clinical response on removal of ligatures and plaque was almost as rapid as the onset. The animal model is useful for manipulating variables in ways not possible in the study of human periodontitis.

Animals↗
PubMed1989

Inhibition of prolyl hydroxylase by poly(ADP-ribose) and phosphoribosyl-AMP. Possible role of ADP-ribosylation in intracellular prolyl hydroxylase regulation.

Poly(ADP-ribose) prepared by incubating NAD+ with rat liver nuclei inhibited the hydroxylation reaction catalyzed by purified prolyl hydroxylase (proline,2-oxoglutarate dioxygenase, EC 1.14.11.2) in vitro. Near complete inhibition of the enzyme was seen in the presence of 6 nM (ADP-Rib)18 with a Ki(app) of 1.5 nM. The monomer unit of poly(ADP-ribose), adenosine diphosphoribose (ADP-Rib), was found to be a weak inhibitor. On the other hand, poly(ADP-ribose)-derived phosphoribosyl-AMP (PRib-AMP) and its dephosphorylated product, ribosyl-ribosyl-adenine (Rib-RibA), inhibited the enzyme in nanomolar concentrations (Ki(app) 16.25 nM). The order of inhibition was (ADP-Rib)18 greater than PRib-AMP, Rib-RibA much greater than ADP-Rib. These results suggested that the 1"----2' ribosyl-ribosyl moiety in these compounds was involved in the inhibition of the enzyme. The possibility that intracellular prolyl hydroxylase is regulated by the involvement of ADP-ribosylation reactions was examined in confluent cultures of skin fibroblast treated with 20 mM lactate. The activity of prolyl hydroxylase was stimulated by 145% over that of untreated cultures. In the lactate-treated cells, the level of NAD+ was lowered and the total ADP-ribosylation of cellular proteins reduced by 40%. These observations imply that the lactate-induced activation of cellular prolyl hydroxylase is mediated by a reduction in ADP-ribosylation and that the synthesis and degradation of ADP-ribose moiety(ies) may possibly regulate prolyl hydroxylase activity in vivo.

Adenosine↗
PubMed1985

Stimulation of poly(ADP-ribose) synthetase activity in the lungs of mice exposed to a low level of ozone.

Toxic effects of O3 are mediated through the formation of free radicals, which can cause DNA strand breaks. Cellular DNA repair is dependent upon the formation of poly(ADP-ribose) (polyADPR) catalyzed by polyADPR synthetase. In order to evaluate whether O3 exposure inflicted DNA damage in lung tissue, we measured the activity of polyADPR synthetase (known to be activated in response to DNA damage) in mouse lungs after exposure to 0.45 ppm (882 micrograms/m3) O3 for up to 7 days. The enzyme activity was stimulated with O3 exposure relative to unexposed controls, showing a 20% (P less than 0.05) increase at Day 5 and 42% (P less than 0.001) at Day 7 of O3 exposure. In addition, the activity of superoxide dismutase (SOD), known to be stimulated in response to production of superoxide anion (.O2-), was measured as an indicator of free radical involvement. Relative to unexposed controls, the SOD activity in exposed animal lungs increased to the peak level at Day 5 (48%, P less than 0.001) and then declined at Day 7 of O3 exposure but was still higher than controls (17%, P less than 0.05). When animals, after 5 days of O3 exposure, were allowed to recover in filtered room air, the activities of both enzymes declined to their respective control values in 6 days. These results suggest a possible temporal relationship between O3 injury and the activities of polyADPR synthetase and a free radical scavenging enzyme, SOD. The stimulation of polyADPR synthetase activity with O3 exposure, reflecting a response to lung cellular DNA repair, may be a sensitive indicator for assessing DNA damage in oxidant injury.

Animals↗
PubMed1985

Poly(ADP-ribose) synthetase activity during bleomycin-induced lung fibrosis in hamsters.

Bleomycin damages cellular DNA and is a potent inducer of pulmonary fibrosis. It has been shown to act through a superoxide-mediated mechanism. We are interested in determining the biochemical mechanisms involved in fibrosis and in this preliminary study we have examined the temporal relationship between early biochemical events associated with DNA damage and fibrosis, in lungs of hamsters after administration of 0.75 unit of bleomycin. The activities of poly(ADP-ribose) synthetase, an enzyme associated with DNA repair, inducible superoxide dismutase (SOD) and prolyl hydroxylase as well as the tissue levels of NAD+ and hydroxyproline in the lung were determined. All three enzyme activities expressed as per milligram DNA or per lung, increased upon bleomycin treatment over the saline-administered controls. Lung poly(ADP-ribose) synthetase activity which is sensitive to DNA breaks, increased first (24% over control in 1 day, P less than 0.0001), attained the maximum value on the 5th day (952% over control, P less than 0.0001), and started to decline thereafter and approached near the control value on 14th day. Bleomycin treatment induced a rapid change in the level of lung NAD+. After 1 day the level of NAD+ was reduced by 42% compared to the control (P less than 0.001), further declined to 65% (P less than 0.001) on the 3rd day, and stayed at that level until the 7th day. On the 14th day, however, the NAD+ level was still lower (29%, P less than 0.05) but approaching the value in the control animals. The activity of prolyl hydroxylase showed significant increase on the 3rd day (50% over control, P less than 0.0001) after bleomycin administration. The enzyme activity continued to increase until the end of the experiment (490% of control, P less than 0.0001, on Day 14). The content of undialyzable hydroxyproline, a marker for collagen, was also increased significantly in the lung tissue on the 3rd day (30% over control, P less than 0.05), continued to increase and reached the highest level on the 14th day (71% over control, P less than 0.001). A significant increase in the activity of SOD (19% over control, P less than 0.001) was seen on the 5th day which continued to increase and attained the highest value on Day 14 (115% over control, P less than 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1978

Macromolecular synthesis in organ cultures of neonatal rat lung.

Organ cultures of newborn rat lungs synthesize and accumulate DNA, RNA, collagen and noncollagenous proteins almost at a linear rate for at least 5 days. During this period the synthesis of collagen consistently exceeds the synthesis of noncollagenous proteins in a pattern similar to neonatal lung growth in vivo. Although some morphological characteristics of lung architecture are distorted after culture, fundamental structural similarities to lungs growing in intact animals are retained. When these cultures are maintained in atmospheres rich in oxygen, increased collagen synthesis is observed, a response similar to that of lungs in intact animals exposed to high oxygen concentrations in vivo. Our studies suggest that lung organ cultures may be a suitable system for investigating the biochemical aspects of lung tissue-environmental interaction.

Animals↗
PubMed1975

Ozone interaction with rodent lung. III. Oxidation of reduced glutathione and formation of mixed disulfides between protein and nonprotein sulfhydryls.

Nonprotein sulfhydryls (NPSH), a major source of cellular reducing substances, were examined in lung tissue after short-term exposure of rats to O3. While the NPSH level was unaffected by low-level exposures (e.g., 0.8 ppm for up to 24 h or 1.5 ppm for up to 8 h), it was significantly lowered by higher exposure regimens (e.g., 25 per cent after 2 ppm for 8 h and 49 per cent after 4 ppm for 6 h). After exposure to 4 ppm O3 for 6 h the level of reduced glutathione (GSH), which accounted for approximately 90 per cent of NPSH in the lung, decreased 40 per cent but without a rise in the level of oxidized gluathione (GSSG). Treatment of lung homogenate with borohydride led to recovery of NPSH in exposed lungs to control values, suggesting that NPSH or GSH oxidation during in vivo O3 exposure resulted in formation of mixed disulfides with other sulfhydryl (SH) groups of lung tissue. Extracts of borohydride-treated particulate and supernatant fractions of lung homogenate were analyzed for NPSH by paper chromatography. From this analysis GSH appeared to be the only NPSH bound to lung tissue proteins via mixed disulfide linkage. The formation of mixed disulfides appeared to be a transient phenomenon. Immediately after a 4-h exposure to 3 ppm O3 the level of mixed disulfides was small (15 per cent of the total NPSH) but attained a peak (equivalent to 0.6 mumol NPSH/lung) after a recovery for 24 h. However, the level diminished considerably within 48 h of recovery.

Animals↗
PubMed1973

Aplastic anemia associated with lithium therapy.

A case is reported of fatal aplastic anemia developing in a 50-year-old woman who received lithium carbonate in the generally accepted dosage for a manic-depressive disorder. The serum lithium had been determined at regular intervals and never exceeded what is considered a safe level. Patients for whom lithium is prescribed should have periodic hematologic examinations.

Anemia, Aplastic↗