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Biomedical subjects

L A Crawford

Publications and source records attributed to L A Crawford.

8 recordsLinked to original sources
PubMed1996

Accumulation and egestion of dietary copper and cadmium by the grasshopper Locusta migratoria R & F (Orthoptera: Acrididae).

Copper and cadmium budgets were studied for a model insect herbivore/host plant system comprising the oligophagous leaf-chewing grasshopper (Locusta migratoria) feeding on Zea mays (Gramineae). Fifth instar larvae were fed, for between 5 and 20 days, on maize foliage contaminated with either copper, cadmium or on control foliage containing no excess metal. Male and female locusts fed on copper-treated maize retained 45 and 42% of ingested copper respectively, figures not significantly different from the 41 and 33% retained on untreated maize. Remaining copper was egested with the faeces. Locusts fed on copper-treated maize showed an increase of 27% in body copper burden compared with those on the control diet: the increase was independent of time on the diet. Female locusts retained 33% and males 21% of ingested cadmium. Faecal cadmium levels were elevated, and accumulation in both sexes was proportional to time on the Cd-enriched diet. For both copper and cadmium, some ingested metal probably passed directly through the locust gut, bound to undigested food material. Results suggest that grasshoppers may effectively regulate excess dietary copper, but are unable efficiently to regulate cadmium.

Journal Article↗
PubMed1993

Incontinence following rupture of the anal sphincter during delivery.

OBJECTIVE: To determine the frequency with which patients report incontinence of flatus or stool after rupture of the anal sphincter during delivery. METHODS: A chart review and telephone interview were conducted with 70 primiparas, 35 of whom had rupture of the anal sphincter at delivery and 35 of whom did not. All were contacted 9-12 months postpartum and questioned about the development of incontinence of gas or liquid or formed stool, persistent dyspareunia, and perineal pain. RESULTS: Incontinence of gas was reported by six women (17%) in the rupture group and one (3%) in the control group (P < .05). The incidence of incontinence of stool, both liquid and solid, dyspareunia, and persistent perineal pain were similar between the groups. CONCLUSION: Incontinence of flatus was reported six times more often by women who experienced a third- or fourth-degree perineal laceration than by those without anal sphincter rupture.

Adult↗
PubMed1990

Hibernation activates glyoxylate cycle and gluconeogenesis in black bear brown adipose tissue.

Biochemical studies on brown adipose tissue removed from a hibernating black bear and a non-hibernating control animal demonstrate that this tissue: (1) can carry out cyanide-insensitive fatty acid oxidation, and (2) possesses catalase activity and the enzyme activities unique to the glyoxylate cycle, isocitrate lyase and malate synthase. These activities are all markedly increased in brown fat obtained from the hibernating animal. Additionally, hibernation enhances the ability of the tissue to synthesize glycogen in the presence of a fatty acid substrate. The glyoxylate cycle enzymes and the ability to convert fatty acid carbons to glucose have been generally regarded as being absent from vertebrate cells and tissues.

Adipose Tissue, Brown↗
PubMed1990

Ethanol induces the generation of reactive free radicals by neural crest cells in vitro.

Developmental craniofacial anomalies related to the neural crest derived ectomesenchymal cell population are associated with fetal alcohol syndrome (FAS). Information regarding any potential relationship between ethanol, free radicals, and the viability, proliferation, etc., of isolated neural crest cells was sought. The hypersensitivity of neural crest cells to ethanol was observed. This drug severely depressed cell viability while simultaneously inducing the generation of such reactive oxygen intermediates (ROI) as superoxide, hydrogen peroxide, and hydroxyl anions. Addition of the free radical scavenging enzyme superoxide dismutase to the culture medium significantly reversed these effects of ethanol. The cytotoxicity of ethanol was further confirmed by the release of radiolabeled chromium (51Cr) from cells prelabeled prior to ethanol treatment. This effect was also depressed by the addition of superoxide dismutase. Interestingly, an assay for superoxide dismutase activity showed that neural crest cells may be devoid of this enzyme. The latter may help to explain the overt sensitivity of these cells to such a broad spectrum of teratogens, many of which can either dissociate directly into ROI, or cause the radicalization of biological structures and molecules. Plasmalemmal lipids (via lipid peroxidation) and DNA are at an especially high risk from uncontrolled ROI. Changes in neural crest cell surface morphology, i.e., loss of microvilli, formation of xeiotic blebs, as well as the "leakage" of radiolabeled Cr from prelabeled cells, would seem to show that ethanol, as a result of induced free radical formation, alters the physiology and biochemistry of the cell membrane. These findings however, should not exclude other potential sites for ETOH-induced cell injury related to free radicals, especially the nuclei (DNA), mitochondria, organelle membranes, and the cytoskeleton.

Animals↗
PubMed1990

Generation of radical oxygen species by neural crest cells treated in vitro with isotretinoin and 4-oxo-isotretinoin.

The effects of isotretinoin (IR) and its primary metabolite (in the human), 4-oxo-isotretinoin (4-OIR or OIR), on isolated chick neural crest cells (NCC's) in culture were studied. NCC's were found to be deficient in both superoxide dismutase (SOD) and catalase, two of the enzymes known to function in the "scavenging" (dismutation) of toxic radical oxygen species (ROS) such as the superoxide anion and hydrogen peroxide. The addition of IR or OIR to the culture medium significantly depressed the viability of the NCC's when compared to untreated cells. OIR was more potent in this regard than IR. In the presence of either IR or OIR, NCC's generated superoxide anions (O2.), hydrogen peroxide (H2O2), and hydroxyl anions (OH.). OIR was again more potent. The cytotoxicity of IR or OIR was demonstrated by the "leakage" of radioactive chromium from prelabeled cells. The latter is suggestive of a primary surface membrane defect, most logically via the induction of lipid peroxides by the retinoids. The latter is accompanied by an increase in membrane permeability and porosity as evidenced by the fact that various fluorescently labeled molecules, including BSA-FITC (MW 69,000), gain entrance into the cytoplasm of the retinoid treated cells. No label was seen in the cytoplasm of similarly treated control cells. When SOD (200 units/ml) or catalase (400 units/ml) was added to the culture media of IR- or OIR-treated NCCs, cell viability was increased and the concentration of the various ROS generated was decreased. Membrane leakiness to chromium and FITC-BSA was also decreased in the presence of these enzymes. Free radicals, when not inactivated (dismutated), are known to be pathobiotic to most cells. Cell membranes are at a particular high risk from ROS which induce structural, physiological, and biochemical alterations in the cell membrane. The latter can have a negative effect on cell permeability, maintenance of normal ionic gradients, membrane enzyme activity, cell-to-cell communication, etc. Such defects can ultimately culminate in hypoplasia, aplasia, and cell necrosis. This study has shown that NCC's may be overtly sensitive to ROS, especially since these undifferentiated cells apparently lack inherent SOD and/or catalase activity. From this study it appears as if both IR and OIR perturb the normal functional state of NCC's by "triggering" the generation of ROS. This may certainly explain the teratogenicity of these drugs as related to the viability of neural crest derived ectomesenchymal cells and normal craniofacial morphogenesis.

Animals↗