Towards the development of a macroinvertebrate sampling technique for palustrine wetlands in South Africa: a pilot investigation in the KwaZuluNatal midlands

A study was undertaken in November 2003 to derive a suitable sampling technique for collecting a representative sample of aquatic macroinvertebrates from a selected emergent vegetation biotope in a palustrine wetland, Melmoth Vlei, KwaZulu-Natal, South Africa. The aim was to undertake a preliminary investigation on the development and testing of a macroinvertebrate sampling technique for use in emergent sedge-dominated palustrine wetlands (sensu Cowardin et al. 1979), which could contribute to the development of a South African wetland health biomonitoring programme. Sweep nets and activity traps were evaluated for their effectiveness in terms of macroinvertebrate collection. Sweep net sampling was tested over a range of sweep intensities to determine the minimum number of sweeps required to collect a representative sample. Sampling efficiency of activity traps placed at four depths was tested, and taxon diversity and composition of sweep net and activity trap samples were compared to determine whether activity traps are required to supplement sweep net data. A total of 32 taxa (identified mainly to family level) were identified in the samples collected. Taxon diversity and composition did not differ in the activity traps placed at the four depth locations. Taxon diversity did not differ significantly between different sweep intensities. This may be a result of high variability of macroinvertebrate distribution within a wetland. There is evidence, however, to suggest that this result is due to an inadequate sample size. There was a significant difference in taxon composition between the different sweep intensities (P < 0.05) and between activity trap and sweep net samples (P < 0.05). Sixty-eight percent of taxa appeared more frequently in sweep net sampling than in activity trap sampling. Two taxa were found exclusively in activity traps, although the numbers of these taxa collected were not significant, and they do not represent any unique trophic group. Based on these findings, it was concluded that activity traps are not required to supplement sweep net data, and a technique using a sweep net with a sweep intensity of five would be suitable for collecting a representative sample of macroinvertebrates from a palustrine wetland.     

Iron homeostasis is maintained in the brain,but not the liver,following mild hypoxia

Abstract

Alterations in iron metabolism or oxidative damage in response to hypoxic incidents have been examined following re-oxygenation of the hypoxic tissue. To understand the consequences of decreased tissue oxygen on iron load, metal-catalyzed redox activity and oxidative modifications in isolation from re-oxygenation, the present study exposed mice to either normoxia, or mild hypoxia (380 Torr; ～10% normobaric oxygen) where the tissue was not allowed to re-oxygenate prior to examination. Brain, liver and skeletal muscle were examined for Fe³⁺ load, metal-catalyzed redox activity and oxidative modifications to proteins (N^?-(carboxymethyl)lysine), lipids (4-hydroxynonenal pyrrole) and nucleic acids (8-hydroxyguanosine). Hypoxia induced a 43% increase in the iron content of the liver (P < 0.001) as determined by ICP-MS and a 3.8-fold increase in Fe³⁺ load (P < 0.001) as determined by Perl's stain. There was a corresponding 2-fold increase in metal-catalyzed redox activity (P < 0.01) in the liver, but no change in the expression of oxidative markers. In contrast, non-significant increases in Fe³⁺ and metal-catalyzed redox activity were observed in the cerebral cortex, and molecular and granular layers of the hippocampus and cerebellum. Interestingly, hypoxia significantly decreased oxidative modifications to proteins and lipids, but not nucleic acids in most brain regions examined. In addition, hypoxia did not alter the Fe content of skeletal muscle, or the contents of Zn, Cu, Ni or Mn in liver, skeletal muscle, cerebral cortex or hippocampus. Together, these results indicate that there is a tighter regulation of iron metabolism in the brain than the liver, which limits the redistribution of Fe³⁺ following hypoxia.     

N-acetylcysteine prevents TNF-induced mitochondrial damage,apoptosis and viral particle production in HIV-infected U937 cells

It has been hypothesized that reactive oxygen intermediates (ROI) can activate human immunodeficiency virus (HIV) replication and that HIV can trigger programmed cell death (PCD). In this work, we studied PCD in U937 cultured cells chronically infected with HIV and exposed to tumor necrosis factor alpha (TNFα). This cytokine has been shown to induce apoptosis in some cell types and to produce intracellular free radical species including ROI. In addition, it was also demonstrated that HIV-induced PCD observable in U937 infected cells can be favored by TNF exposure. In one of our recent works, evidence was presented that the thiol supplier N-acetylcysteine (NAC) can ‘protect’, at least partially, HIV-infected cells from PCD and determine a significant decrease in viral progeny. In the present work, we demonstrate (a) that apoptosis can be easily induced by TNF only in infected U937 cells and not in control wild-type cells, (b) that daily treatment of TNF-exposed cells with low concentrations of NAC is able to impair viral progeny formation as early as 24 h, (c) that the mitochondrial damage induced by TNF is counteracted by preexposure to NAC, and (d) that NAC alone exerts changes in mitochondria which may be responsible for the protective effects exerted by this compound. Because of the radical producing capacity of TNF, these results seem to indicate that the protective effects of NAC may be due to the specific antioxidant nature of this substance which appears to be capable of impairing both the apoptotic machinery and viral replication by an intracellular mechanism involving mitochondrial integrity and function.