The influence of parasitism on wing development in male and female pea aphids.

Wing formation in presumptive alate morphs (virginoparae and males) was observed for the pea aphid, Acyrthosiphon pisum, exposed to attack by the parasitoid, Aphidius ervi, at different stages of host development. Morphological abnormalities in parasitized aphids such as complete apterization (development of a wingless form), formation of rudimentary wing buds, and deformed wings indicate a possible disruption of the endocrine system. Changes in the body shape and the number of olfactory secondary rhinaria on the antennae could indicate an influence of juvenile hormone in parasitized A. pisum but the development of fifth-stadium supernumerary larvae (indicated by an extra moult and which can be induced by exogenous juvenile hormone treatments) was not found in parasitized aphids. In addition, while apterization of virginoparae can also be induced by the pro-allatocidal compound Precocene III, this was not possible in the male. Males which survived parasitoid attack without forming aphid mummies (indicating that oviposition had not occurred) developed as wingless individuals suggesting that the reproductive-tract-fluids from the female parasitoid were important in the wing inhibition process. Teratocytes from the parasitoid appeared to promote developmental arrest in parasitized aphids.

Environmental and physiological factors for diapause induction and termination in the aphid parasitoid, Aphidius ervi (Hymenoptera: Aphidiidae).

In the aphid parasitoid Aphidius ervi Haliday, the incidence of diapause around the critical photoperiod was dependent on temperature. At a photoperiod of 12 h light:12 h dark, a significantly higher proportion of diapausing individuals was found at 12 degrees C than at 15 degrees C. The second larval stage of the parasitoid was most sensitive to photoperiod and localised-illumination experiments showed that the parasitoid responded independently of the aphid host. The sex ratio of the population which emerged after rearing in short-days and/or after diapause was male biased. Topical application of the juvenile hormone-mimic, pyriproxyfen, before or during diapause delayed emergence of Aphidius ervi but did not induce diapause or influence its termination. The ecdysteroid mimic RH 5849 induced diapause in a few treated individuals but did not affect diapause termination.

Detection of polycyclic aromatic hydrocarbon exposure damage using different methods in laboratory animals.

Benzo[a]pyrene, benzo[b]fluoroanthene and dibenzo[a,h]anthracene dissolved in a 1:2 mixture of dimethylsulphoxide (DMSO) and water were administered to two groups of female mice, each group containing 15 mice. The doses were administered orally (via gavage) at the respective rates of 1 and 100 micrograms kg-1 body weight five times per week for a period of 9 weeks. The influence of the polycyclic aromatic hydrocarbons (PAHs) was determined using the following methods: determination of DNA-PAH adducts, of chromosome injuries (micronucleus test), of induction of repair using the unscheduled DNA synthesis (UDS) test, and by examination of the DNA structure after nucleoid sedimentation. All the methods investigated provided evidence of a significant effect resulting from exposure to PAHs on the parameters examined. Following chronic exposure to PAHs, the formation of DNA-PAH adducts and injury to the genetic material, as well as the appearance of micronuclei (micronucleus test), the induction of unscheduled DNA synthesis (UDS test) and mutation of the DNA structure (nucleoid sedimentation), were demonstrated. The described methods therefore provide a means for the detection of genetic damage caused by PAH exposure in humans.

UDS-test with freon 11 (R-11).

Trichlorofluoromethane, in concentrations of 80, 400, 2 000, 10 000 and 50 000 ppm, was administered to rats of both sexes (Sprague Dawley) by inhalation exposure.2 000 ppm in air (= 11 200 mg/m(3)) amount to twice the MAK value of 1 000 ppm. At exposure times of 4 hours this corresponds to the MAK value defined for an 8 hour workday.Unscheduled DNA synthesis (UDS) was measured in single-cell suspensions of hepatocytes, pulmonary epithelial cells and lymphocytes of the spleen, respectively.In the pulmonary cells concentrations of 2 000, 10 000 and 50 000 ppm of freon 11 lead to a significantly increased mean silver grain count compared to a negative control group.In spleen and liver cells increasing concentrations of R 11 tend to increase the incorporation of thymidine into the DNA of the cells. These changes of the extent of unscheduled DNA synthesis can, however, not be statistically verified.

Continuous induction of unscheduled DNA synthesis by gamma irradiation.

The induction of DNA-synthesis in non-S-phase cells is a very sensitive measure of a preceding damage of DNA. Usually, in an in vivo-in vitro test (treatment of an animal, incorporation of H3-thymidine in a cell suspension) the damaging of DNA takes place hours to days before the evaluation. In this case, the time course of the UDS-induction after a single dose of 1 Gy gamma irradiation was observed over a long period of time (21 months). C57 black mice served as test animals. In an age of about 80 days they were irradiated and the induction of unscheduled DNA synthesis was measured at ten time intervals during the whole life-span of the animals. Although the repair in this gamma radiation damage in DNA is a very quick process--with centrifugation in alkaline sucrose a half-life of some minutes is found--an induction of unscheduled DNA synthesis could be seen at the irradiated animals until the end of their life (640 days). The reason for this could be permanent disorders in cellular regulation caused by the gamma irradiation.

Influence of nicotine on DNA metabolism.

We investigated the influence of nicotine and its metabolites on semiconservative DNA synthesis, DNA repair processes, and the rejoining of DNA strand breaks. Using a combined treatment with nicotine and gamma irradiation and counting the number of sister chromatid exchanges, we evaluated the action of nicotine on the whole DNA repair process, especially examining the possibility that DNA is damaged by the action of nicotine. All tests were performed on HeLa cells and verified with human lung fibroblasts. Liver microsomes of aroclor-treated rats were used as the metabolizing agent. Our findings showed that nicotine and its metabolites at concentrations below 1 mmol/l are not toxic in the cell lines used and within this subtoxic range they have no effect on DNA metabolism. Neither was DNA repair obstructed after gamma irradiation nor did the number of sister chromatid exchanges increase.

A comparison of the photochemical actions of 5- and 8-methoxypsoralen on CHO cells.

Chinese Hamster ovary (CHO) cells were treated with 5- or 8-methoxypsoralen (MOP) in combination with longwave UV light (UVA). The toxicity and the action of these substances on DNA synthesis as well as well as the nature of damage caused by them in combination with UVA light and the ability of the cells to repair this damage was examined. 8-MOP induces interstrand crosslinks within the DNA when applied together with UVA light. It decreases the rate of DNA synthesis at sublethal doses. 5-MOP shows the same effect though it induces virtually no DNA crosslinks. The repair of damage process. It is not quite complete at 24 h. Neither compound has an effect on CHO cells when applied without UVA light.

[The action of hyperthermia on DNA repair (author's transl)]. / Die Wirkung von Hyperthermie auf DNA-Reparaturvorgänge.

The time-course of DNA repair after gamma irradiation was measured in HeLa cells at various temperatures. Unscheduled DNA synthesis was estimated by incorporation of 3H-thymidine in presence of hydroxyurea. To detect the ligase reaction, the number of single strand breaks (SSB) was determined by centrifugation in alcaline sucrose as well as by hydroxylapatite chromatography after partial denaturation. In addition, the temperature dependence of DNA polymerase and DNase reaction in cell-free systems were measured. These data were compared with the reduction of colony-forming ability of the cells caused by gamma irradiation and following repair at various temperatures. All steps of repair proceed faster at 41--43 degrees than at 37 degrees but cells are most resistant to gamma irradiation at 37 degrees. We therefore assume that the DNA repair process at 42 degrees is faster but more error prone than at 37 degrees.