Compartmental analysis of sulphate transport in Lemna minor L., taking plant growth and sulphate metabolization into consideration

Rat hepatoma cells accumulate considerably less 2-aminoisobutyrate after cultivating in the absence of serum the change in rate of aminoisobutyrate uptake takes place within 1 h of serum starvation. Starvation of amino acids by contrast raises aminoisobutyrate uptake in the presence or absence of serum, but the cells are much less responsive to amino acid supply than to availability of serum. Phosphate (10 mM) reduced aminoisobutyrate uptake by cells grown in serum to that exhibited by serum-starved cells. Aminoisobutyrate uptake by cells grown in serum was reduced by glycine, proline, alanine, serine, glutamine, methylaminoisobutyrate and 2-aminonorbornane-2-carboxylate, the effects of methylaminoisobutyrate and 2-aminonorbornane-2-carboxylate being additive. However, similar inhibition phenomena were not seen for cells deprived of serum where aminoisobutyrate uptake tended to a relatively constant level insensitive to inhibitory influences, yet substantially greater than that arising by simple diffusion. The comparative insensitivity of our hepatoma line when starved of serum to competition and repression phenomena is in contrast to findings of others. Our results also suggest a lack of clear delineation of specificities for the A and L transport systems as usually defined.     

Gold Nanoparticle Interference Study during the Isolation,Quantification, Purity and Integrity Analysis of RNA

Investigations have been conducted regarding the interference of nanoparticles (NPs) with different toxicological assay systems, but there is a lack of validation when conducting routine tests for nucleic acid isolation, quantification, integrity, and purity analyses. The interference of citrate-capped gold nanoparticles (AuNPs) was investigated herein. The AuNPs were added to either BEAS-2B bronchial human cells for 24 h, the isolated pure RNA, or added during the isolation procedure, and the resultant interaction was assessed. Total RNA that was isolated from untreated BEAS-2B cells was spiked with various concentrations (v/v%) of AuNPs and quantified. A decrease in the absorbance spectrum (220–340 nm) was observed in a concentration-dependent manner. The 260 and 280 nm absorbance ratios that traditionally infer RNA purity were also altered. Electrophoresis was performed to determine RNA integrity, but could not differentiate between AuNP-exposed samples. However, the spiked post-isolation samples did produce differences in spectra (190–220 nm), where shifts were observed at a shorter wavelength. These shifts could be due to alterations to chromophores found in nucleic acids. The co-isolation samples, spiked with 100 µL AuNP during the isolation procedure, displayed a peak shift to a longer wavelength and were similar to the results obtained from a 24 h AuNP treatment, under non-cytotoxic test conditions. Moreover, hyperspectral imaging using CytoViva dark field microscopy did not detect AuNP spectral signatures in the RNA isolated from treated cells. However, despite the lack of AuNPs in the final RNA product, structural changes in RNA could still be observed between 190–220 nm. Consequently, full spectral analyses should replace the traditional ratios based on readings at 230, 260, and 280 nm. These are critical points of analyses, validation, and optimization for RNA-based techniques used to assess AuNPs effects.     

Oxygen free radical scavenger enzyme polymorphisms in systemic sclerosis

We performed a case-control study of polymorphisms of glutathione S-transferase (GST) isoenzymes and manganese superoxide dismutase (MnSOD) in black South Africans with systemic sclerosis (SSc). The frequency of the GSTM1*B phenotype was significantly decreased in the overall SSc group compared with controls (OR=0.19, p(corr)<.05), implying a possible protective effect against development of the disease. There was also a trend toward increased MnSODAla allele and phenotype frequencies in the diffuse cutaneous SSc subset compared with controls (OR=2.11 and 3.15, respectively, p(corr)<.1). Our findings provide new data on the distribution of GST and MnSOD polymorphisms in healthy Africans and further evidence that genetic factors may have a contributory role to play in predisposing to oxidative stress in SSc.     

Antioxidant and genotoxic properties of South African herbal extracts

This study investigated the antioxidant and genotoxic properties of 13 South African herbal extracts. Results from the single-cell gel electrophoresis (Comet) assay indicated that there were profound differences between the plant extracts in their ability to produce DNA damage, which varied from highly genotoxic to protective. Similarly, water and methanol extracts of all the herbal preparations showed variable potencies in scavenging hydroxyl radicals, as measured by means of electron spin resonance spectrometery (ESR) with the spin trap alpha-phenyl-N-tert-butylnitrone (PBN). In general, methanol extracts were better scavengers of hydroxyl radicals than the corresponding water extracts. This was also true of the ability of these extracts to inhibit membrane lipid peroxidation, assessed with diphenyl-1-pyrenylphosphine (DPPP). However, neither methanol nor water extracts had the ability to protect against DNA damage. The results show that further research on South African traditional herbal extracts is imperative to gain understanding of the mechanisms involved in their pharmacological effects. The tests implemented in the present investigation are recommended for screening other herbal extracts.     

Hydroxyl radical production in the presence of fibres by a Fenton-type reaction

Glass fibres are considered to be inert and therefore thought to present no real hazard to the health of people who inhale them. Results in the present study however indicate that these fibres are able to produce hydroxyl radicals in the presence of hydrogen peroxide by a Fenton-type reaction. Since hydroxyl radical is implicated in lipid peroxidation, single-strand DNA breaks and carcinogenesis, care should be exercised when dealing with glass fibres.     

DNA methylation similarities in genes of black South Africans with systemic lupus erythematosus and systemic sclerosis

Background

Systemic lupus erythematosus (SLE) and systemic sclerosis (SSc) are systemic autoimmune connective tissue diseases that share overlapping clinico-pathological features. It is highly probable that there is an overlap in epigenetic landscapes of both diseases. This study aimed to identify similarities in DNA methylation changes in genes involved in SLE and SSc. Global DNA methylation and twelve genes selected on the basis of their involvement in inflammation, autoimmunity and/or fibrosis were analyzed using PCR arrays in three groups, each of 30 Black South Africans with SLE and SSc, plus 40 healthy control subjects.

Results

Global methylation in both diseases was significantly lower (<25 %) than in healthy subjects (>30 %, p = 0.0000001). In comparison to healthy controls, a similar gene-specific methylation pattern was observed in both SLE and SSc. Three genes, namely; PRF1, ITGAL and FOXP3 were consistently hypermethylated while CDKN2A and CD70 were hypomethylated in both diseases. The other genes (SOCS1, CTGF, THY1, CXCR4, MT1-G, FLI1, and DNMT1) were generally hypomethylated in SLE whereas they were neither hyper- nor hypo-methylated in SSc.

Conclusions

SSc and SLE patients have a higher global hypomethylation than healthy subjects with specific genes being hypomethylated and others hypermethylated. The majority of genes studied were hypomethylated in SLE compared to SSc. In addition to the commonly known hypomethylated genes in SLE and SSc, there are other hypomethylated genes (such as MT-1G and THY-1) that have not previously been investigated in SLE and SSc though are known to be hypermethylated in cancer.     

Challenges and Research Needs for Risk Assessment of Pesticides for Registration in Africa

Risk assessment is necessary for registration and risk management of new pesticides. The aim of this article is to discuss challenges that risk assessors in Africa face when conducting risk assessment of pesticides. Risk assessment requires toxicity assessment, environmental fate studies, and the use of models for occupational, dietary, residential, and environmental exposure assessments. Toxicity studies are very costly with the result that toxicity data used to register pesticides in Africa are often sourced from northern hemisphere countries. Assessors also often use exposure modeling results from the northern hemisphere. This is not an ideal approach as occupational exposure is influenced by agricultural practices, climatic conditions, and other factors. Furthermore, residential exposure models require time-location-activity information, exposure factors, and toxicokinetic rate constants for particular pesticides. Dietary exposure assessment needs accurate and comprehensive local food consumption data. Authorities in African countries should therefore generate the required data, despite these being very costly and tedious. Authorities should also provide guidance on the type of models and standard scenarios for estimating predicted environmental concentrations in various environmental compartments. It is recommended that higher educational institutions in Africa should incorporate risk assessment in general and pesticide toxicity and exposure models in particular in their curricula.     

Systematic Review of Screening and Surveillance Programs to Protect Workers from Nanomaterials

BackgroundScreening and surveillance approaches for workers exposed to nanomaterials could aid in early detection of health effects, provide data for epidemiological studies and inform action to decrease exposure. The aim of this review is to identify such screening and surveillance approaches, in order to extract available data regarding (i) the studies that have successfully been implemented in present day, (ii) identification of the most common and/or toxic nano-related health hazards for workers and (iii) possible exposure surveillance markers. This review contributes to the current understanding of the risk associated with nanomaterials by determining the knowledge gap and making recommendations based on current findings.MethodsA systematic review was conducted. PubMed and Embase were searched to identify articles reporting on any surveillance-related study that described both exposure to nanomaterials and the health indicators that were measured. Four reviewers worked in pairs to independently assess the eligibility of studies and risk of bias before extraction of data. Studies were categorised according to the type of study and the medical surveillance performed, which included the type of nanomaterial, any exposure details provided, as well as health indicators and biomarkers tested.ResultsInitially 92 studies were identified, from which 84 full texts were assessed for eligibility. Seven studies met all the inclusion criteria, i.e. those performed in Taiwan, Korea, Czech Republic and the US. Of these, six compared health indicators between exposed and unexposed workers and one study described a surveillance program. All studies were at a high risk of bias. Workers were exposed to a mix of nanomaterials in three studies, carbon-based nanomaterials in two studies, nano-silver in one study and nano-titanium oxide in the other study. Two studies did not find a difference in biomarkers between exposed and unexposed workers. In addition, differences in early effects on pulmonary function or neurobehavioral tests were not observed. One study found an increased prevalence of allergic dermatitis and “sneezing” in the exposed group.ConclusionsThis review of recently published data on surveillance studies proves that there is a gap in the current knowledge, where most of the surveillance-related studies reported do not follow a set format that provides the required information on ENM characterisation, the type of exposure and the measured indicators/biomarkers. Hence, there is very low quality evidence that screening and surveillance might detect adverse health effects associated with workplace exposure. This systematic review is relevant because it proves that, although surveillance programs have been initiated and preliminary results are being published, the current studies are actually not answering the important questions or solving the overall problem regarding what the potential health hazards are among workers either handling or potentially exposed to ENMs. The recommendations, thus proposed, are based on an obvious need for (i) exposure registries, where longitudinal follow-up studies should inform surveillance, (ii) known exposure measurements or summary indices for ENMs as a reference (iii) validation of candidate biomarkers and (iv) studies that compare the effects of these surveillance approaches to usual care, e.g. those commonly followed for bulk-size hazardous materials.     

The ability of mineral dusts and fibres to initiate lipid peroxidation. Part II: relationship to different particle-induced pathological effects

Exposure to pathogenic mineral dusts and fibres is associated with pulmonary changes including fibrosis and cancer. Investigations into aetiological mechanisms of these diseases have identified modifications in specific macromolecules as well as changes in certain early processes, which have preceded fibrosis and cancer. Peroxidation of lipids is one such modification, which is observed following exposure to mineral dusts and fibres. Their ability to initiate lipid peroxidation and the parameters that determine this ability have recently been reviewed. Part II of this review examines the relationship between the capacity of mineral dusts and fibres to initiate lipid peroxidation and a number of pathological changes they produce. The oxidative modification of polyunsaturated fatty acids is a major contributor to membrane damage in cells and has been implicated in a great variety of pathological processes. In most pathological conditions where an induction of lipid peroxidation is observed it is assumed to be the consequence of disease, without further establishing if the induction of lipid peroxidation may have preceded or accompanied the disease. In the great majority of instances, however, despite the difficulty in proving this association, a causal relationship between lipid peroxidation and disease cannot be ruled out.