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Biomedical subjects

J Reddy

Publications and source records attributed to J Reddy.

106 records · Page 6Linked to original sources
PubMed1971

Hepatic megalocytosis in chronic lasiocarpine poisoning. Some functional studies.

In an attempt to understand the nature of cytoplasmic and nuclear enlargement of liver cells designated as megalocytosis that results from chronic poisoning by lasiocarpine, a pyrrolizidine alkaloid, certain functional aspects of these cells were investigated together with the study of their morphology. The RNA polymerase activity of the megalocyte nuclei was essentially comparable to the activity observed in normal liver cells. Further, the inducibility of tryptophan pyrrolase activity by hydrocortisone, in the livers of rats treated chronically with lasiocarpine is an indication that translational mechanisms are intact. However, the increased uptake of 3H-thymidine by megalocytes, in the absence of observable mitotic activity, suggests that these cells are in the process of hypertrophy. It is concluded that the megalocytes are functionally normal cells, except that they are in the process of cellular hypertrophy and are incapable of division due to potent antimitotic action of the pyrrolizidine alkaloids.

Alkaloids↗
PubMed1969

Microbodies in experimentally altered cells. II. The relationship of microbody proliferation to endocrine glands.

The liver cells of intact male rats given ethyl-alpha-p-chlorophenoxyisobutyrate (CPIB) characteristically show a marked increase in microbodies and in catalase activity, while those of intact female rats do not. In castrated males given estradiol benzoate and CPIB the increase in catalase activity and microbody proliferation is abolished, while in castrated females given testosterone propionate and CPIB the livers show a marked increase in microbodies and in catalase activity. No sex difference in microbody and catalase response is apparent in fetal and neonatal rats. Both sexes show a sharp rise in catalase activity on the day of birth, with a rapid decline at 5 days after birth. Thyroidectomy abolishes the hypolipidemic effect of CPIB in rats, but microbody proliferation and increase in catalase activity persists in thyroidectomized male rats, indicating that microbody proliferation can be independent of hypolipidemia. Adrenalectomy does not alter appreciably the microbody-catalase response to CPIB. These experiments demonstrate that (1) in adult rats, hepatic microbody proliferation is dependent to a significant degree upon male sex hormone but is largely independent of thyroid or adrenal gland hormones; (2) hepatic microbody proliferation is independent of the hypolipidemic effect of CPIB; (3) displacement of thyroxine from serum protein may not be sufficient cause for stimulation of microbody formation.

Adrenalectomy↗
PubMedDate not supplied

Role of arachidonic acid metabolites in tumor growth inhibition by nonsteroidal antiinflammatory drugs.

PURPOSE: A murine model of squamous cell carcinoma (SCC) was used to determine the role of arachidonic acid (AA) metabolites in the growth of SCC of the head and neck. MATERIALS AND METHODS: C3H/HeJ mice bearing SCC (SCC VII) were treated with cyclooxygenase inhibitors (piroxicam and nabumetone) or a 5-lipoxygenase inhibitor (ketoconazole). Growth curves were established, and final tumor weights were measured. Following sacrifice, tumor tissue homogenates were assayed for prostaglandin E2 (PGE2) and 12-hydroxyeicosatetraenoic acid (12-HETE) by enzyme-linked immunosorbent assay (ELISA), and leukotriene B4 (LTB4) by radioimmunoassay (RIA). Inflammatory cell infiltrate was assessed histologically. RESULTS: A significant inhibition of tumor growth (P = .001) and final tumor weight (P = .002) was noted in mice treated with piroxicam and nabumetone. Inhibition of tumor growth was associated with increased tumor tissue levels of PGE2 (P = .04) and lymphocytic infiltration (P = .07). Significant inhibition of tumor growth (P = .002) and final tumor weight (P = .05) was also noted in mice treated with ketoconazole. CONCLUSION: These data suggest that both cyclooxygenase and lipoxygenase metabolites of AA affect tumor growth in this model and that inhibition of tumor growth by inhibitors of AA metabolism may be caused by an enhanced inflammatory cell response at the tumor site.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMedDate not supplied

Scale-up studies on a defined medium process for pilot plant production of illicicolin by Gliocladium roseum.

Illicicolin was cultivated at the 600-L pilot scale for purposes of material generation and process development. The initial medium containing oat flour was difficult operationally as a result of excessive foaming during sterilization, so a new defined medium process (with either glucose or sucrose as the carbon source), developed at the 23-L scale, was scaled up and improved for pilot scale needs. Pilot scale media development efforts focused on exploring the highest concentration of media (1.0 x to 3.0 x) that could be cultivated at the pilot scale and not be limited by mixing or oxygen mass transfer. The process was scaled up successfully and peak titers improved 7.5-fold, from about 200 mg/L in the initial complex medium to 1500 mg/L in the final defined medium.

Fermentation↗