Nanotoxicological evaluation of oxidative responses in rat nephrocytes induced by cadmium

Hamdi Trabelsi, Inès Azzouz, Soumaya Ferchichi, Olfa Tebourbi, Mohsen Sakly, Hafedh Abdelmelek Laboratory of Integrative Physiology, Faculty of Sciences of Bizerte, Carthage University, Jarzouna, Tunisia Abstract: The aim of this study was to investigate the interaction of cadmium chloride with mineral elements in rat nephrocytes in terms of the biosynthesis of nanocomplexes. The results show that selenium supplementation enhanced cadmium accumulation in kidneys. Analysis of the fluorescence revealed an increase in red fluorescence in the kidneys of rats co-exposed to cadmium and selenium. Interestingly, X-ray diffraction measurements carried out on kidney fractions of co-exposed rats point to the biosynthesis of cadmium selenide and/or sulfide nanoparticles (about 62 nm in size). Oxidative stress assays showed the ability of selenium to reduce lipid peroxidation and to restore glutathione peroxidase and superoxide dismutase activity in kidneys. Hence, cadmium complexation with selenium and sulfur at a nanoscale level could reduce oxidative stress induced by cadmium in kidneys. Keywords: nanoparticles, detoxification, oxidative stress, X-ray diffraction, fluorescence microscopy, kidney

Interaction between nanoparticles generated by zinc chloride treatment and oxidative responses in rat liver

Inès Azzouz, Hamdi Trabelsi, Amel Hanini, Soumaya Ferchichi, Olfa Tebourbi, Mohsen Sakly, Hafedh AbdelmelekLaboratory of Integrative Physiology, Faculty of Sciences of Bizerte, Carthage University, TunisiaAbstract: The aim of the present study was to investigate the interaction of zinc chloride (3 mg/kg, intraperitoneally [ip]) in rat liver in terms of the biosynthesis of nanoparticles. Zinc treatment increased zinc content in rat liver. Analysis of fluorescence revealed the presence of red fluorescence in the liver following zinc treatment. Interestingly, the co-exposure to zinc (3 mg/kg, ip) and selenium (0.20 mg/L, per os [by mouth]) led to a higher intensity of red fluorescence compared to zinc-treated rats. In addition, X-ray diffraction measurements carried out on liver fractions of zinc-treated rats point to the biosynthesis of zinc sulfide and/or selenide nanocomplexes at nearly 51.60 nm in size. Moreover, co-exposure led to nanocomplexes of about 72.60 nm in size. The interaction of zinc with other mineral elements (S, Se) generates several nanocomplexes, such as ZnS and/or ZnSe. The nanocomplex ZnX could interact directly with enzyme activity or indirectly by the disruption of mineral elements' bioavailability in cells. Subacute zinc or selenium treatment decreased malondialdehyde levels, indicating a drop in lipid peroxidation. In addition, antioxidant enzyme assays showed that treatment with zinc or co-treatment with zinc and selenium increased the activities of glutathione peroxidase, catalase, and superoxide dismutase. Consequently, zinc complexation with sulfur and/or selenium at nanoscale level could enhance antioxidative responses, which is correlated to the ratio of number of ZnX nanoparticles (X=sulfur or X=selenium) to malondialdehyde level in rat liver.Keywords: nanocomplexes biosynthesis, antioxidative responses, X-ray diffraction, fluorescence microscopy, live

Evaluation of oxidative response and tissular damage in rat lungs exposed to silica-coated gold nanoparticles under static magnetic fields

Soumaya Ferchichi,1 Hamdi Trabelsi,1 Inès Azzouz,1 Amel Hanini,2 Ahmed Rejeb,3 Olfa Tebourbi,1 Mohsen Sakly,1 Hafedh Abdelmelek1 1Laboratory of Integrative Physiology, Faculty Of Sciences of Bizerte, 2Laboratory of Vascular Pathology, Carthage University, Carthage 3Laboratory of Pathological Anatomy, National School of Veterinary Medicine of Sidi Thabet, Manouba Univeristy, Manouba, Tunisia Abstract: The purpose of our study was the evaluation of toxicological effects of silica-coated gold nanoparticles (GNPs) and static magnetic fields (SMFs; 128 mT) exposure in rat lungs. Animals received a single injection of GNPs (1,100 µg/kg, 100 nm, intraperitoneally) and were exposed to SMFs, over 14 days (1 h/day). Results showed that GNPs treatment induced a hyperplasia of bronchus-associated lymphoid tissue. Fluorescence microscopy images showed that red fluorescence signal was detected in rat lungs after 2 weeks from the single injection of GNPs. Oxidative response study showed that GNPs exposure increased malondialdehyde level and decreased CuZn-superoxide dismutase, catalase, and glutathione peroxidase activities in rat lungs. Furthermore, the histopathological study showed that combined effects of GNPs and SMFs led to more tissular damages in rat lungs in comparison with GNPs-treated rats. Interestingly, intensity of red fluorescence signal was enhanced after exposure to SMFs indicating a higher accumulation of GNPs in rat lungs under magnetic environment. Moreover, rats coexposed to GNPs and SMFs showed an increased malondialdehyde level, a fall of CuZn-superoxide dismutase, catalase, and glutathione peroxidase activities in comparison with GNPs-treated group. Hence, SMFs exposure increased the accumulation of GNPs in rat lungs and led to more toxic effects of these nanocomplexes. Keywords: malondialdehyde, catalase, superoxide dismutase, glutathione peroxidase, bronchus-associated lymphoid tissue, nanotoxicity, histopathological stud

Age modulates Fe3O4 nanoparticles liver toxicity: dose-dependent decrease in mitochondrial respiratory chain complexes activities and coupling in middle-aged as compared to young rats.

International audienc

Biomed Res Int

We examined the effects of iron oxide nanoparticles (IONPs) on mitochondrial respiratory chain complexes activities and mitochondrial coupling in young (3 months) and middle-aged (18 months) rat liver, organ largely involved in body iron detoxification. Isolated liver mitochondria were extracted using differential centrifugations. Maximal oxidative capacities (V(max), complexes I, III, and IV activities), V(succ) (complexes II, III, and IV activities), and V tmpd, (complex IV activity), together with mitochondrial coupling (V(max)/V0) were determined in controls conditions and after exposure to 250, 300, and 350 mu g/ml Fe3O4 in young and middle-aged rats. In young liver mitochondria, exposure to IONPs did not alter mitochondrial function. In contrast, IONPs dose-dependently impaired all complexes of the mitochondrial respiratory chain in middle-aged rat liver: V(max) (from 30 +/- 1.6 to 17.9 +/- 1.5; P < 0.001), V(succ) (from 33.9 +/- 1.7 to 24.3 +/- 1.0; P < 0.01), V(tmpd) (from 43.0 +/- 1.6 to 26.3 +/- 2.2 micromol O2/min/g protein; P < 0.001) using Fe3O4 350 microg/ml. Mitochondrial coupling also decreased. Interestingly, 350 mu g/ml Fe3O4 in the form of Fe(3+) solution did not impair liver mitochondrial function in middle-aged rats. Thus, IONPs showed a specific toxicity in middle-aged rats suggesting caution when using it in old age