The protection of selenium on adriamycin-induced mitochondrial damage in rat

Although adriamycin (ADR) exhibits high anti-tumor efficacy in vitro, its clinical use in cancer chemotherapy is limited due to its high renal toxicity. This study investigated the mechanism of ADR nephropathy and the protective effect of selenium on ADR-induced kidney damage by analyzing of the relationship between selenium and mitochondria. Rats were divided into four groups. The first group was injected with saline i.p. for 21 days, the second group received the 4 mg/kg i.p. ADR every alternate day for 8 days, the third group received the 50 μg/kg i.p. Se for 21 days, and the fourth group received the Se. ADR co-administration i.p. blood pressures were assessed, the mitochondrial membrane potential (MMP) was assessed, and the adenosine triphosphate (ATP) levels were determined. The total antioxidant (TAS) and oxidant status (TOS) in cytosol, the mitochondria of kidney cells, and plasma were measured. Mitochondrial TAS decreased and TOS increased in the ADR group compared to the Se group. ADR-treated rats showed significantly lower MMP than did the control and Se groups. MMP was significantly restored in the Se + ADR group through selenium treatment compared to the ADR group (p < 0.01). In the ADR group, a reduction in ATP content was seen compared to the control and Se groups (p < 0.01). ATP level was significantly restored through treatment with selenium in the Se + ADR group compared to the ADR group (p < 0.01). We concluded that selenium is effective in vivo against ADR-induced kidney damage via the restoration of TAS and TOS, which prevented mitochondrial damage.     

Founder mutations in Tunisia: implications for diagnosis in North Africa and Middle East

ABSTRACT: Background Tunisia is a North African country of 10 million inhabitants. The native background population is Berber. However, throughout its history, Tunisia has been the site of invasions and migratory waves of allogenic populations and ethnic groups such as Phoenicians, Romans, Vandals, Arabs, Ottomans and French. Like neighbouring and Middle Eastern countries, the Tunisian population shows a relatively high rate of consanguinity and endogamy that favor expression of recessive genetic disorders at relatively high rates. Many factors could contribute to the recurrence of monogenic morbid trait expression. Among them, founder mutations that arise in one ancestral individual and diffuse through generations in isolated communities. Method We report here on founder mutations in the Tunisian population by a systematic review of all available data from PubMed, other sources of the scientific literature as well as unpublished data from our research laboratory. Results We identified two different classes of founder mutations. The first includes founder mutations so far reported only among Tunisians that are responsible for 30 genetic diseases. The second group represents founder haplotypes described in 51 inherited conditions that occur among Tunisians and are also shared with other North African and Middle Eastern countries. Several heavily disabilitating diseases are caused by recessive founder mutations. They include, among others, neuromuscular diseases such as congenital muscular dystrophy and spastic paraglegia and also severe genodermatoses such as dystrophic epidermolysis bullosa and xeroderma pigmentosa. Conclusion This report provides informations on founder mutations for 73 genetic diseases either specific to Tunisians or shared by other populations. Taking into account the relatively high number and frequency of genetic diseases in the region and the limited resources, screening for these founder mutations should provide a rapid and cost effective tool for molecular diagnosis. Indeed, our report should help designing appropriate measures for carrier screening, better evaluation of diseases burden and setting up of preventive measures at the regional level.     

High Fill Factor Polymer Solar Cells Incorporating a Low Temperature Solution Processed WO3 Hole Extraction Layer

We demonstrate solution‐processed tungsten trioxide (WO₃) incorporated as hole extraction layer (HEL) in polymer solar cells (PSCs) with active layers comprising either poly(3‐hexylthiophene) (P3HT) or poly[(4,4'‐bis(2‐ethylhexyl)dithieno[3,2‐b:2′,3′‐d]silole)‐2,6‐diyl‐alt‐(4,7‐bis(2‐thienyl)‐2,1,3‐benzothiadiazole)‐5,50‐diyl] (Si‐PCPDTBT) mixed with a fullerene derivative. The WO₃ layers are deposited from an alcohol‐based, surfactant‐free nanoparticle solution. A short, low‐temperature (80 °C) annealing is sufficient to result in fully functional films without the need for an oxygen‐plasma treatment. This allows the application of the WO₃ buffer layer in normal as well as inverted architecture solar cells. Normal architecture devices based on WO₃ HELs show comparable performance to the PEDOT:PSS reference devices with slightly better fill factors and open circuit voltages. Very high shunt resistances (over 1 MΩ cm²) and excellent diode rectification underline the charge selectivity of the solution‐processed WO₃ layers.     

Bromophenol blue binding as a probe to study urea and guanidine hydrochloride denaturation of bovine serum albumin

Urea and guanidine hydrochloride (GdnHCl) denaturation of bovine serum albumin (BSA) were investigated using bromophenol blue (BPB) binding as a probe. Addition of BPB to BSA produced an absorption difference spectrum in the wavelength range, 525-675 nm with a minimum at 587 nm and a maximum at 619 nm. The magnitude of absorption difference (DeltaAbs.) at 619 nm decreased on increasing urea/GdnHCl concentration and followed the denaturation curve. The denaturation was found to be a two-state, single-step transition. The transitions started at 1.75 and 0.875 M and completed at 6.5 and 3.25 M with the mid point occurring around 4.0 and 1.5 M urea and GdnHCl concentrations, respectively. The value of free energy of stabilization, DeltaGDH2O as determined from urea and GdnHCl denaturation curves was found to be 4041 and 4602 cal/mol, respectively. Taken together, these results suggest that BPB binding can be used as a probe to study urea and GdnHCl denaturation of BSA.     

Age, growth, mortality and population structure of the oyster, Crassostrea madrasensis, in the Moheskhali Channel (southeastern coast of Bangladesh)

The population structure, age, growth, mortality and harvest intensity of the oyster Crassostrea madrasensis were examined in the Moheskhali Channel, Bangladesh between June 2003 and May 2004. The channel is a representative habitat for the area. C. madrasensis monthly length frequency data were analyzed using FiSAT software for estimating population parameters, including asymptotic length ( L _∝ ), growth co-efficient ( K ) and recruitment pattern to assess the status of the stock. Asymptotic length ( L∝ ) and growth co-efficient ( K ) were 20.88 cm and 0.35 year⁻¹, respectively. The growth performance index (φ') was calculated with 2.18. The growth pattern showed negative allometric growth ( b  < 3), with an asymptotic weight ( W _∝ ) of about 1124.6 g. The oyster attained an average length of 6.17 cm at the end of 1 year. Total mortality ( Z ) by length-converted catch curve was estimated at 1.78 year⁻¹, fishing mortality ( F ) at 0.77 year⁻¹, and natural mortality ( M ) at 1.01 year⁻¹. The exploitation level ( E ) of C. madrasensis was 0.43, while the maximum allowable limit of exploitation ( E _max) was 0.45 for the highest yield. The recruitment pattern was continuous, displaying a single major peak event per year. Habitat temperatures were 25.5–31.0°C (mean ± SD, 29 ± 1.62°C); salinity range was from 12.36 to 26.0 ppt (mean ± SD, 19.6 ± 4.7 ppt). The exploitation level (0.43) indicated that the oyster stock was exploited at almost maximum yield in this channel.     

原代培养过程中壳聚糖衍生物对CTCF/YB-1/C-myc和p53蛋白表达的影响

成功建立了人增生性瘢痕细胞和正常皮肤成纤维细胞的原代培养, 并利用热休克蛋白(HSP47)和成纤维细胞特异蛋白(FSP)标记物进行了鉴定。研究发现, 经过壳聚糖衍生物处理, 人增生性瘢痕成纤维细胞和正常皮肤成纤维细胞在培养中均出现了不同类型的蛋白表达。多功能转录因子蛋白(CTCF)在壳聚糖衍生物处理的增生性瘢痕成纤维细胞中出现表达上调; 在聚糖衍生物处理的正常皮肤成纤维细胞中数量无变化。YB-1结合蛋白在经壳聚糖处理的正常皮肤成纤维细胞与人增生性瘢痕细胞中的表达几乎无异, 但在未经壳聚糖处理的细胞中表达不同。C-MYC和P53蛋白在壳聚糖衍生物处理的增生性瘢痕纤维细胞中表达上调, 但在正常皮肤成纤维细胞中, 无论是否经过壳聚糖衍生物处理, 这两种蛋白都没有表达。上述4种蛋白在人增生性瘢痕细胞和正常皮肤成纤维细胞中表现出不同的表达方式, 这种新型壳聚糖衍生物可能在控制人增生性瘢痕细胞和正常皮肤成纤维细胞生长和增殖过程中起着重要作用。这些蛋白因子的表达机制目前还不是完全清楚, 有待于进一步研究。     

Thermal responses of Durum wheat Triticum durum to early water stress. Consequence on leaf and flower development

Drought can alter stem apex temperature and plant phenological development and it can then have an effect on the duration of the durum wheat stages. Thermal responses of plants to water stress are tentatively analysed as regards microclimate conditions by applying three different water treatments. Apex temperature measurements showed that they are related to radiation and that acceleration of apex development could be related to their increase.     

Sodium meta-arsenite induced reactive oxygen species in human red blood cells: impaired antioxidant and membrane redox systems,haemoglobin oxidation,and morphological changes

Arsenic (As) is an air and water toxicant that causes cancer in multiple organs. Humans are exposed to As through contaminated water. We have examined the cytotoxicity of sodium meta-arsenite (SA), an As(III) compound, in human red blood cells (RBC) under in vitro conditions. Haemolysates were prepared from human RBC treated with different concentrations of SA (0.1–5.0?mM) for 5?h at 37?°C. SA treatment of RBC caused significant increase in methaemoglobin formation, protein and lipid oxidation, and nitric oxide levels. It also resulted in decrease in glutathione levels, methaemoglobin reductase activity and plasma membrane redox system. SA exposure also inhibited the pathways of glucose metabolism while increasing AMP deaminase and glyoxalase-I. It impaired the enzymatic and non-enzymatic antioxidant defence systems which resulted in decreased antioxidant power and a compromised ability to quench free radicals. SA exposure also damaged the membrane since it decreased the activity of membrane bound enzymes, increased the osmotic fragility of treated cells and induced gross morphological changes. This cytotoxicity was the result of oxidative damage since the production of reactive oxygen species (ROS) was increased in SA treated erythrocytes. Thus As(III) causes extensive damage to RBC which impairs their antioxidant system and alters the major cellular metabolic pathways. All this has the potential to lower the oxygen carrying capacity of RBC and reduce their lifespan in blood.