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At least 577 records · Page 32Linked to original sources
PubMed1984

Ascaris lumbricoides and Ascaridia galli: biogenic amines in adults and developmental stages.

Ascaris lumbricoides var. hominis and Ascaridia galli contain 5-hydroxytryptamine, histamine, dopamine, and norepinephrine. The chick parasite showed lower levels of monoamines compared to human ascaris. Amine concentrations in females were higher than in males. In all specimens, 5-hydroxytryptamine was the highest while norepinephrine was found to be uniformly low. The female reproductive organ contained the maximum amount of dopamine while intestine was rich in histamine. A progressive increase in the concentrations of biogenic amines was noticed during development.

Animals↗
PubMed1983

Spectrophotometric analyses of hydroxysteroid dehydrogenase activity in presumed steroid-producing tissues of the brook lamprey (Lampetra planeri bloch) in different developmental stages.

Hydroxysteroid dehydrogenase (HSD) activity was determined spectrophotometrically on homogenates of the pronephros, the opisthonephros, and the gonads of metamorphosing, immature, and mature adult male and female brook lampreys (Lampetra planeri Bloch), employing pregnenolone, dehydroepiandrosterone, androsterone, epiandrosterone, and 3 beta,17 beta-dihydroxy-5 alpha-androstane as substrates and NAD or NADP as coenzymes in October, December, February, and April. With NADP a higher HSD-dependent HSD activity was detected in presumed adrenocortical tissue (PAT) homogenates with pregnenolone and 3 beta,17 beta-dihydroxy-5 alpha-androstane and in gonad homogenates only with 3 beta,17 beta-dihydroxy-5 alpha-androstane. With 3 beta,17 beta-dihydroxy-5 alpha-androstane as substrate the highest enzyme activities were measured in PAT and gonad homogenates from animals of all investigated life stages. A varying intensity of HSD activity in the examined tissue homogenates probably dependent on stages of the individual development was observed.

3-Hydroxysteroid Dehydrogenases↗
PubMed1989

Effect of praziquantel on the migration and survival of developmental stages of Schistosoma mansoni in mice.

Compressed organ autoradiography has been used to determine whether the anthelmintic drug praziquantel (Pzq) modifies the migration of isotopically labelled Schistosoma mansoni during the first 16 days of infection in CBA/Ca mice. The mice were treated with 500 mg kg-1 body weight of the drug on day 1 or day 6. Treatment caused a marked delay in parasite migration from the skin when the drug was administered intradermally at the site of infection on day 1; migration from the lungs was also delayed after such treatment. Pzq injected either intradermally on day 1 or intramuscularly on day 6 effectively reduced the number of parasites that finally arrived in the lungs and the livers by 41 and 47%, respectively. Intramuscular administration of the drug on day 1 had a negligible effect. Worm recoveries assessed on day 38 by perfusion of the hepatic portal system were greatly reduced when Pzq was administered on day 14. The worms proved less susceptible when the drug was administered on day 21 and were completely resistant following drug delivery on day 28. The influence of drug preparation and route of delivery on parasite migration and survival are discussed.

Animals↗
PubMedDate not supplied

Comparative studies of the induction of somatic eye-color mutations in an unstable strain of Drosophila melanogaster by MMS and X-rays at different developmental stages.

An unstable white locus in Drosophila melanogaster originally described by Rasmuson and Green (1974) and further by Rasmuson et al. (1978, 1980) contains an IS element. This constellation interacts with the zeste mutation and forms a mutationally unstable system that is sensitive to a variety of mutagens. Mutational shifts between zeste and wild-type eye color as well as deletions and transpositions of the white locus are frequently occurring in the unstable X-chromosome in germ line and in somatic tissue. Germinal mutations from zeste to wild-type eye color are associated with an insertion of a piece of DNA, proximal to the wsp site, and the shifts from red to zeste are caused by an excision of the same piece (Rasmuson, in preparation). Mutations to pigmentless phenotype are interpreted as deletions of the white locus, while they always are irreversible and show non-complementation with wsp. The somatic system can be used as a screening test for potential mutagens, described by Rasmuson et al. (1984). This survey is an attempt to correlate the size of the mutated area of the eyes with the age of the larvae at mutagen treatment. X-Rays and MMS were used to give an indication of the mechanism of the instability, according to the different kinds of DNA damage induced. The results show that the mean size of red spots decreased with increasing age of larvae at treatment, while the mutation frequencies were increased because of the multiplication of the cells in the eye anlage susceptible to the mutagens. This is contradictory to the hypothesis maintained by Fahmy and Fahmy (1980) that the somatic shifts are not mutagenic but epigenetic events, due to altered regulation of the gene expression. Red spots induced with MMS are smaller in size than X-ray-induced red spots, indicating a delay in the establishment of mutations from chemically-induced lesions compared to irradiation damage. White spots on the other hand were equally large in size, irrespective of inducing agent and about twice the size of the chemically-induced red spots, implying a faster and more direct action for fixation of deletions than for the production of MMS induced shifts in eye color from zeste to red.

Age Factors↗
PubMed1986

Developmental stage specificity and dose response of secalonic acid D-induced cleft palate and the absence of cytotoxicity in developing mouse palate.

Incidence of cleft palate (CP) in full-term mouse fetuses was evaluated following administration of 25 mg/kg of the mycotoxin, secalonic acid D (SAD), to groups of female mice on each of Days 10, 11, 12, 13, 14, or 15 of pregnancy. Although the highest numerical incidence (45.3%) of cleft palate resulted following SAD exposure on Day 12 of pregnancy, and the response tapered off to 16.9% on Day 10 and 0% on Day 15 of pregnancy, similar responses were produced also following exposures on Days 11 (38.4%) and 13 (39.9%) of pregnancy. Maternal exposure to doses of 0, 15, 20, 25, or 30 mg/kg of SAD, given on Day 12 of pregnancy indicated that although fetuses in the 30-mg/kg group had the highest incidence (51.9%) of CP, the effect was associated with increased resorptions and decreased fetal weights. The 25-mg/kg dose was optimally teratogenic (45.3% cleft palate) and maximally tolerable with neither an increase in resorptions nor a decrease in fetal body weights. Cytotoxicity of the optimally teratogenic dose of SAD (25 mg/kg given ip) on Day 12 of pregnancy was evaluated as a possible mechanism of SAD teratogenicity using indices such as mesenchymal cell density, mitotic index, and the uptake of [3H]thymidine in the developing palatal shelves. No evidence of SAD cytotoxicity was obtained in palatal shelves indicating a possible role for nonlethal cellular effects of SAD in the pathogenesis of CP. These studies also suggest the suitability of the maternal 25-mg/kg dose of SAD to study cellular biochemical effects in the developing embryo without the complicating influence of cytotoxic effects.

Animals↗
PubMed1993

Toxicity of the venom from Nasonia vitripennis (Hymenoptera: Pteromalidae) toward fly hosts, nontarget insects, different developmental stages, and cultured insect cells.

A venom preparation from Nasonia vitripennis, a wasp ectoparasitoid of fly pupae, was assayed for lethality in different stages of insects representing ten different orders and in cultured insect cells. In most cases, the motor activity of the injected insects remained completely normal for 1-2 days after the injection and displayed none of the symptoms of paralysis commonly reported for venoms of the Hymenoptera. A natural host, the flesh fly Sarcophaga bullata, was highly sensitive in the pupal stage (LD50 = 5.4 and 5.5 VRE/g for nondiapausing and diapausing pupae, respectively), the stage that is normally parasitized, and larvae and adults were as susceptible to the venom as the pupae. Adults of another fly host, Phaenicia sericata, were nearly as sensitive (LD50 = 6.5 VRE/g), but nonhost adult flies were more tolerant. Among the other orders tested, pupae of several species (Plodia interpunctella, Trichoplusia ni, Tenebrio molitor) were more susceptible to envenomation than larval or adult stages. In fact, the highest sensitivity observed in this study (LD50 = 0.58 VRE/g) was with pupae of the cabbage looper, T. ni, a species that is not a natural host. In contrast, the larvae (LD50 = 7.23 VRE/g) and adults (LD50 = 7.48) of T. ni were far less sensitive. Adults of Nasonia vitripennis were not sensitive to their own venom (LD50 = > 533 VRE/g), although adults of another hymenopteran, Apis mellifera, were suceptible (4.62 VRE/g). Adults of Lymantria dispar, Oncopeltus fasciatus, Aphis nerii, Euborellia annulipes, Diapheromera femorata, Blattella germanica, Periplaneta americana, and Reticulitermes flavipes demonstrated a high tolerance to Nasonia venom. When tested in vitro, the venom caused cultured Lepidoptera (TN-368) and Diptera (NIH SaPe4) cells to round up, swell, and eventually die. The LC50S were 0.0014 and 0.0010 VRE/microliters for TN-368 and SaPe4 cells, respectively. Cytotoxicity was observed within 10 min after exposure to LC99 levels of venom, with 100% cell mortality at 100 min for the NIH SaPe4 cells and 24 hr for TN-368 cells. It is possible that the venom component responsible for in vivo and in vitro activities may be different, but results from the cell culture work suggest that this method offers a promising assay for quickly screening venom samples. The high susceptibility of flies and pupae of other insects to the venom, as well as its novel (nonparalytic) action suggest that it may have considerable potential for development as a biopesticide.

Animals↗