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Kharroubi A Gargouri D Baati H Azri C 《Environmental monitoring and assessment》2012,184(6):4001-4014
Concentrations of selected heavy metals (Cd, Pb, Zn, Cu, Mn, and Fe) in surface sediments from 66 sites in both northern and
eastern Mediterranean Sea–Boughrara lagoon exchange areas (southeastern Tunisia) were studied in order to understand current
metal contamination due to the urbanization and economic development of nearby several coastal regions of the Gulf of Gabès.
Multiple approaches were applied for the sediment quality assessment. These approaches were based on GIS coupled with chemometric
methods (enrichment factors, geoaccumulation index, principal component analysis, and cluster analysis). Enrichment factors
and principal component analysis revealed two distinct groups of metals. The first group corresponded to Fe and Mn derived
from natural sources, and the second group contained Cd, Pb, Zn, and Cu originated from man-made sources. For these latter
metals, cluster analysis showed two distinct distributions in the selected areas. They were attributed to temporal and spatial
variations of contaminant sources input. The geoaccumulation index (I
geo) values explained that only Cd, Pb, and Cu can be considered as moderate to extreme pollutants in the studied sediments. 相似文献
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Rajeh Caroline Saoud Imad P. Kharroubi Samer Naalbandian Salpy Abiad Mohamad G. 《Journal of Material Cycles and Waste Management》2021,23(1):1-17
Journal of Material Cycles and Waste Management - While society struggles to meet increasing food demand and mitigate food security challenges, approximately one-third of the food produced globally... 相似文献
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Wafa Kharroubi Madiha Dhibi Manel Mekni Zohra Haouas Imed Chreif Fadoua Neffati Mohamed Hammami Rachid Sakly 《Environmental science and pollution research international》2014,21(20):12040-12049
Six groups of rats (n?=?10 per group) were exposed to 1 and 10 mg/l of sodium arsenate for 45 and 90 days. Kidneys from treated groups exposed to arsenic showed higher levels of trans isomers of oleic and linoleic acids as trans C181n-9, trans C18:1n-11, and trans C18:2n-6 isomers. However, a significant decrease in eicosenoic (C20:1n-9) and arachidonic (C20:4n-6) acids were observed in treated rats. Moreover, the “Δ5 desaturase index” and the saturated/polyunsaturated fatty acids ratio were increased. There was a significant increase in the level of malondialdehyde at 10 mg/l of treatment and in the amount of conjugated dienes after 90 days (p?0.05). Significant kidney damage was observed at 10 mg/l by increase of plasma marker enzymes. Histological studies on the ultrastructure changes of kidney supported the toxic effect of arsenate exposure. Arsenate intoxication activates significantly the superoxide dismutase at 10 mg/l for 90 days, whereas the catalase activity was markedly inhibited in all treated groups (p?0.05). In addition, glutathione peroxidase activity was significantly increased at 45 days and dramatically declined after 90 days at 10 mg/l (p?0.05). A significant increase in the level of glutathione was marked for the groups treated for 45 and 90 days at 1 mg/l followed by a significant decrease for rats exposed to 10 mg/l for 90 days. An increase in the level of protein carbonyl was observed in all treated groups (p?0.05). In conclusion, the present study provides evidence for a direct effect of arsenate on fatty acid (FA) metabolism which concerns the synthesis pathway of n-6 polyunsaturated fatty acids and leads to an increase in the trans FAs isomers. Therefore, FA-induced arsenate kidney damage could contribute to trigger kidney cancer. 相似文献
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Wafa Kharroubi Madiha Dhibi Zohra Haouas Imed Chreif Fadoua Neffati Mohamed Hammami Rachid Sakly 《Environmental science and pollution research international》2014,21(3):1648-1657
The present study aimed to evaluate the effect of arsenic on liver fatty acids (FA) composition, hepatotoxicity and oxidative status markers in rats. Male rats were randomly devised to six groups (n?=?10 per group) and exposed to sodium arsenate at a dose of 1 and 10 mg/l for 45 and 90 days. Arsenate exposure is associated with significant changes in the FA composition in liver. A significant increase of saturated fatty acids (SFA) in all treated groups (p?<?0.01) and trans unsaturated fatty acids (trans UFA) in rats exposed both for short term for 10 mg/l (p?<?0.05) and long term for 1 and 10 mg/l (p?<?0.001) was observed. However, the cis UFA were significantly decreased in these groups (p?<?0.05). A markedly increase of indicator in cell membrane viscosity expressed as SFA/UFA was reported in the treated groups (p?<?0.001). A significant increase in the level of malondialdehyde by 38.3 % after 90 days of exposure at 10 mg/l was observed. Compared to control rats, significant liver damage was observed at 10 mg/l of arsenate by increasing plasma marker enzymes after 90 days. It is through the histological investigations in hepatic tissues of exposed rats that these damage effects of arsenate were confirmed. The antioxidant perturbations were observed to be more important at groups treated by the high dose (p?<?0.05). An increase in the level of protein carbonyls was observed in all treated groups (p?<?0.05). The present study provides evidence for a direct effect of arsenite on FA composition disturbance causing an increase of SFA and TFAs isomers, liver dysfunction and oxidative stress. Therefore, arsenate can lead to hepatic damage and propensity towards liver cancer. 相似文献
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Wafa Kharroubi Samia Haj Ahme Thomas Nury Pierre Andreoletti Rachid Sakly Mohamed Hammami Gérard Lizard 《环境科学学报(英文版)》2017,29(1):44-51
The treatment of microglial BV-2 cells with sodium arsenate(As(V):0.1-400 μmol/L — 48 hr)induces a dose-dependent response.The neurotoxic effects of high concentrations of As(V)(100,200 and 400 μmol/L) are characterized by increased levels of mitochondrial complexesⅠ,Ⅱ,and Ⅳ followed by increased superoxide anion generation.Moreover,As(V) triggers an apoptotic mode of cell death,demonstrated by an apoptotic SubG1 peak,associated with an alteration of plasma membrane integrity.There is also a decrease in transmembrane mitochondrial potential and mitochondrial adenosine triphosphate ATP.It is therefore tempting to speculate that As(V) triggers mitochondrial dysfunction,which may lead to defective oxidative phosphorylation subsequently causing mitochondrial oxidative damage,which in turn induces an apoptotic mode of cell death. 相似文献
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