Invertebrate responses to the management of genetically modified herbicide-tolerant and conventional spring crops. I. Soil-surface-active invertebrates.

The effects of herbicide management of genetically modified herbicide-tolerant (GMHT) beet, maize and spring oilseed rape on the abundance and diversity of soil-surface-active invertebrates were assessed. Most effects did not differ between years, environmental zones or initial seedbanks or between sugar and fodder beet. This suggests that the results may be treated as generally applicable to agricultural situations throughout the UK for these crops. The direction of the effects was evenly balanced between increases and decreases in counts in the GMHT compared with the conventional treatment. Most effects involving a greater capture in the GMHT treatments occurred in maize, whereas most effects involving a smaller capture were in beet and spring oilseed rape. Differences between GMHT and conventional crop herbicide management had a significant effect on the capture of most surface-active invertebrate species and higher taxa tested in at least one crop, and these differences reflected the phenology and ecology of the invertebrates. Counts of carabids that feed on weed seeds were smaller in GMHT beet and spring oilseed rape but larger in GMHT maize. In contrast, collembolan detritivore counts were significantly larger under GMHT crop management.

Invertebrate responses to the management of genetically modified herbicide-tolerant and conventional spring crops. II. Within-field epigeal and aerial arthropods.

The effects of the management of genetically modified herbicide-tolerant (GMHT) crops on the abundances of aerial and epigeal arthropods were assessed in 66 beet, 68 maize and 67 spring oilseed rape sites as part of the Farm Scale Evaluations of GMHT crops. Most higher taxa were insensitive to differences between GMHT and conventional weed management, but significant effects were found on the abundance of at least one group within each taxon studied. Numbers of butterflies in beet and spring oilseed rape and of Heteroptera and bees in beet were smaller under the relevant GMHT crop management, whereas the abundance of Collembola was consistently greater in all GMHT crops. Generally, these effects were specific to each crop type, reflected the phenology and ecology of the arthropod taxa, were indirect and related to herbicide management. These results apply generally to agriculture across Britain, and could be used in mathematical models to predict the possible long-term effects of the widespread adoption of GMHT technology. The results for bees and butterflies relate to foraging preferences and might or might not translate into effects on population densities, depending on whether adoption leads to forage reductions over large areas. These species, and the detritivore Collembola, may be useful indicator species for future studies of GMHT management.

Biochemical studies on rabbits with aluminium induced neurofilament accumulations.

The activities of acid phosphatase, hexosaminidase, beta-galactosidase, Mg2+-stimulated Na+K+ATPase, fumarase and ATP:citrate lyase were measured in grey matter of rabbit spinal cord 7-8 days after intra-ventricular or intra-cisternal injection of aluminium. RNA, DNA, and water content were measured in whole spinal cords. Choline acetyltransferase (CAT) and acetylcholinesterase were assayed in dorsal grey matter of the cord, which contained no aluminium-induced neurofilament accumulations (NFAs), and ventral grey matter, which had large numbers of such NFAs. CAT was also assayed in the hypoglossal nerve. None of these measures were consistently altered in the aluminium treated rabbits, although the activity of beta-galactosidase was increased in the NFA-free caudate nucleus of rabbits given aluminium intra-ventricularly, possibly due to the presence of phagocytes on the ventricular surface of the caudate. It is concluded that neither aluminium nor its induced NFAs has a gross effect on neuronal metabolism within 7-8 days.

Intoxication with four synthetic pyrethroids fails to show any correlation between neuromuscular dysfunction and neurobiochemical abnormalities in rats.

The neurological effects of four synthetic pyrethroids resmethrin, permethrin, cypermethrin, and deltamethrin have been investigated in the rat to establish whether there is a correlation between the clinical-functional status of the animal and peripheral nerve damage as measured biochemically. Neuromuscular dysfunction was assessed by means of the inclined plane test and peripheral nerve damage by reference to beta-glucuronidase and beta-galactosidase activity increases in nerve tissue homogenates from treated and control animals. A transient functional impairment was found in animals treated with any one of the four pyrethroids tested and in all cases this was maximal at the end of the 7 day subacute dosing regimen. Significant increases in beta-glucuronidase and beta-galactosidase were found 3-4 weeks after the start of dosing in the distal portion of the sciatic/posterior tibial nerves from permethrin, cypermethrin, and deltamethrin treated animal; but no changes were found in remesthrin-dosed animals. It is concluded therefore, that there is no direct correlation between the time-course of the neuromuscular dysfunction and the neurobiochemical changes. This suggests that these pyrethroids have at least two distinct actions--a short-term pharmacological effect and at near-lethal dose levels a more chronic neurotoxic effect that results in sparse axonal nerve damage.

Protection against misonidazole-induced neuropathy in rats: a biochemical assessment.

A biochemical method for assessing the chemically induced neurotoxicity of misonidazole (MISO) in the rat has been used to assess whether the concurrent administration of thiamine, thiamine pyrophosphate (TPP) or vitamin E (Vit.E) could afford protection against the neurotoxic side effects of the drug. The tissues analysed were distal sections of the sciatic/posterior tibial nerve (SPTN), trigeminal ganglia and cerebellum. MISO was administered i.p. to Wistar rats at a dose of 400 mg/kg per day for 7 consecutive days to produce the maximal measurable enzyme changes after 4 weeks. The concurrent i.p. and i.m. dosing of thiamine (0.1-100 mg/kg) for 15 consecutive days did not abate the subsequent PNS and CNS enzyme changes. However, with concurrent i.m. dosing of 1.0 mg/kg TPP or p.o. dosing of vitamin E (30 mg/kg) afforded some protection against both the PNS and CNS MISO-induced neurotoxic side effects as measured biochemically.

A biochemical assessment of the neurotoxicity of the radiosensitizing drug misonidazole in the rat.

We have obtained biochemical evidence that misonidazole when administered in large doses to rats produces a sparse dying-back peripheral neuropathy and degenerative changes in the trigeminal ganglia and cerebellum. In our experience these neurotoxic effects of misonidazole cannot be detected reliably by the use of simple behavioural and functional tests, e.g., inclined plane and narrowing bridge tests (Rose and Dewar, unpublished results). Therefore, these methods would be of limited use in the neurotoxicity screening of misonidazole analogues. On the other hand, the biochemical approach provides a convenient quantitative method which could be used as the basis for comparing the neurotoxicity of other candidate radiosensitizing drugs.

A biochemical method for assessing the neurotoxic effects of misonidazole in the rat.

A proven biochemical method for assessing chemically induced neurotoxicity has been applied to the study of the toxic effects of misonidazole (MISO) in the rat. This involves the fluorimetric measurement of beta-glucuronidase and beta-galactosidase activities in homogenates of rat nervous tissue. The tissues analysed were sciatic/posterior tibial nerve (SPTN) cut into 4 sections, trigeminal ganglia and cerebellum. MISO administered i.p. to Wistar rats in doses greater than 300 mg/kg/day for 7 consecutive days produced maximal increases in both beta-glucuronidase and beta-galactosidase activities in th SPTN at 4 weeks (140-180% of control values). The highest increases were associated with the most distal secretion of the nerve. Significant enzyme-activity changes were also found in the trigeminal ganglia and cerebellum of MISO-dosed rats. The greatest activity occurred 4-5 weeks after dosing, and was dose-related. It is concluded that, in the rat, MISO can produce biochemical changes consistent with a dying-back peripheral neuropathy, and biochemical changes suggestive of cerebellar damage. This biochemical approach would appear to offer a convenient quantitative method for the detection of neurotoxic effects of other potential radio-sensitizing drugs.

The role of retinol in, and the action of anti-inflammatory drugs on, hereditary retinal degeneration.

Light deprivation retarded retinal degeneration in albino dystrophic rats. In pigmented dystrophic rats the presence of pigment in the eye retarded the degenerative process. Retinol labilized rat retinal lysosomes in vitro. Acetylsalicylic acid stabilized retinal lysosomes even in the presence of the concentration of retinol which produced the maximum labilization. The effect of acetylsalicyclic acid was concentration dependent, maximum stabilization being produced by 0.25-0.50 mM. The results provide further evidence for the hypothesis that hereditary retinal degeneration in rats is mediated by an increased amount of retinol (produced by the action of light on an unusually labile type of visual pigment) causing a premature release of lysosomal enzymes.