Toxicology and Industrial Health

Hallegue, Dorsaf ;Tebourbi, Olfa ;Kacem, Kamel ;Sakly, Mohsen ;Rhouma, Khémaïs Ben

doi: 10.1177/0748233710362373pmid: 20185541

The current study deals with the effect of the organochlorine insecticide on the liver of Wistar rats. The dieldrin effect on rats was tested after a single intraperitoneal (i.p.) injection of two doses: 3 and 6 mg/kg and observations were made 4 days later. Animals showed a significant dose-dependent increase in relative liver weight. Elevations of transaminases (aspartate aminotransferase [AST], alanine aminotransferase [ALT]), bilirubin and total activity of lactate dehydrogenase (LDH) were recorded in the sera of treated rats. Serum LDH-5 isoenzyme activity increases in a dose-dependent manner. In contrast, LDH-1 activity does not show any significant variations with respect to controls. Histological examination of the liver of dieldrin-treated animals revealed cytoplasmic vacuolation, focal necrosis and nuclear enlargement of hepatocytes. This study suggests that biochemical assessment (transaminases, LDH and bilirubin activity) and LDH (LDH-1 & LDH-5) isoenzyme profiles can be very helpful in defining the border of the liver injury, dieldrin damaged liver would be a valuable addition to histological analysis in evaluating histopathological liver changes.

Borg, Damon Andrew ;Trombetta, Louis David

doi: 10.1177/0748233710362381pmid: 20176777

This investigation studied the acute effects of copper pyrithione (CuPT) exposure on juvenile brook trout, Salvelinus fontinalis. Morphologic changes, copper bioaccumulation, and markers of oxidative stress in gill tissue were studied. Juvenile brook trout were treated with one of six experimental doses of CuPT (2—64 μg/L) for 2 hours. A seventh group served as a control population. Inductively coupled plasma atomic absorbance spectrophotometry (ICPAAS) analysis demonstrates significantly increased levels of copper in gill tissue (p < 0.001). Results from scanning electron microscopy and histological analysis demonstrate the formation of club-shaped lamella, edema, fusion of secondary lamella, loss of microridge structures and epithelial exfoliation. Transmission electron microscopy revealed altered morphology of chloride cells, including the swollen appearance of mitochondria with disruption of internal cristae and lipid membrane disruption. Thiobarbituric acid reactive substance (TBARS) assays demonstrated increased levels of lipid peroxidation products in gill tissue. Assays for the total antioxidant capacity of gill tissue revealed significantly lowered antioxidant levels. This data indicates that CuPT is potentially harmful to nontarget aquatic organisms at environmentally relevant doses.

Qiu, Shuiqing;Huang, Shuling;Huang, Juan;Pan, Jianlin;Zhang, Weiyun

doi: 10.1177/0748233710362376pmid: 20176778

As a freshwater pearl mussel, Hyriopsis cumingii is widely cultured in China to produce pearls. This study was made to explore the antitumor activity of water-soluble polysaccharide (WSP) from mantles of H. cumingii. Cell viability of human hepatocarcinoma HepG2 cells was estimated by MTT method. Cell cycle analysis was determined by flow cytometry. Apoptosis was observed under fluorescence microscopy and confirmed by DNA fragment assay. Reverse transcriptase-polymerized chain reaction (RT-PCR) and immunocytochemistry were carried to evaluate c-myc, bcl-2 and cyclinD1 gene expressions in HepG2 cells. Furthermore, intracellular reactive oxygen species (ROS) production was assessed by flow cytometry. After WSP treatment, the growth of HepG2 cells was inhibited and most of cells arrested in G0/G1 phage (p < .01); apoptotic changes in nucleus and cytoplasm were also observed in WSP-treated cells; percentage of apoptotic rate significantly increased in a dose-dependent manner (p < 0.001); DNA fragmentation was detected in treated HepG2 cells; The mRNA level and protein level of c-myc, bcl-2 and cyclinD1 were decreased in the treated HepG2 cells. ROS was significantly increased in a dose- and time-dependent manner as well. The results suggested that WSP has potent antitumor activity.

Durante, Paula ;Romero, Freddy ;Pérez, Mariela ;Chávez, Maribel ;Parra, Gustavo

doi: 10.1177/0748233710362377pmid: 20176775

Oxidative stress is an important mechanism in mercury poisoning. We studied the effect of uric acid, a natural and potent reactive oxygen species and peroxynitrite scavenger, in HgCl 2-induced nephrotoxicity. Rats were injected with a unique dose of HgCl2 (2.5 mg/kg body weight, subcutaneously) and then vehicle (for 3 days, twice daily) or HgCl2 (unique dose) and intraperitoneal uric acid suspension (250 mg/kg body weight, twice daily, for 3 days), and then killed at 24, 48 and 72 hours after HgCl2 administration (n = 5 for each group). At the end of the experimental study, kidneys and blood samples were taken. Tissues were prepared and examined under light microscopy. Uric acid significantly prevented the increase in plasma levels of creatinine and blood urea nitrogen (BUN); it helped maintain systemic nitrate/nitrite concentration and total antioxidant capacity. Uric acid attenuated the increase of renal lipid peroxidation and it markedly diminished nitrotyrosine signal and histopathological changes as early as 24 hours after HgCl2 administration. Uric acid did not prevent a decrease in β-actin signal caused by mercuric chloride, but it promoted a faster recovery when compared to the HgCl2 alone group. Our results indicate that UA could play a beneficial role against HgCl2 toxicity by preventing systemic and renal oxidative stress and tissue damage.

Pekmez, Hidir ;Ogeturk, Murat ;Ozyurt, Huseyin ;Sonmez, Mehmet Fatih ;Colakoglu, Neriman ;Kus, Ilter

doi: 10.1177/0748233710362380pmid: 20176779

It was aimed to investigate the histopathological and biochemical changes in kidney tissues of rats exposed to cigarette smoke and possible protective effects of caffeic acid phenethyl ester (CAPE) on these changes. Twenty one male Wistar albino rats were divided into three equal groups. Animals in group I were used as control. Rats in group II were exposed to cigarette smoke and rats in group III were exposed to cigarette smoke and daily administration of CAPE. At the end of the 60-day experimental period, all the animals were sacrificed by decapitation. The serum samples obtained from the animals were studied for uric acid, creatinine and blood urine nitrogen (BUN) levels. Following routine histological procedures, kidney tissue specimens were examined under a light microscope. In addition, dismutase (SOD) and glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) and nitric oxide (NO) contents were determined spectrophotometrically in tissue samples. It was found that serum uric acid and BUN levels of the rats exposed to cigarette smoke alone were elevated, although serum creatinine levels did not significantly change. Furthermore, renal SOD, GSH-Px, NO and MDA levels were significantly increased. These increases in serum BUN, and renal SOD, GSH-Px, NO and MDA levels were significantly inhibited by CAPE treatment. In light microscopic observations of tissues from rats exposed to smoke, mesangial cell proliferation in the renal corpuscles, dilatation and congestion in the peritubular capillaries and degenerative alterations in the proximal tubules were noted. There were also atrophic renal corpuscles. However, these histopathological changes were partially disappeared in the rats exposed to cigarette smoke plus CAPE. The present findings indicate that cigarette smoke causes impairment in renal structure and function, which can be prevented by CAPE administration.

Iavicoli, Ivo ;Bocca, Beatrice ;Fontana, Luca ;Caimi, Stefano ;Bergamaschi, Antonio ;Alimonti, Alessandro

doi: 10.1177/0748233710362383pmid: 20176776

This study determined the distribution in internal organs and the elimination routes in rats after oral administration of potassium hexachloro-palladate. Forty male Wistar rats were exposed for 90 days to 0, 10, 100 and 250 ng/mL of the palladium (Pd) salt in drinking water. Samples of urine and feces were collected on days 1, 30, 60 and 90, while organs (kidney, liver, lung, spleen and bones) and blood were collected at the end of the experiment. Quantification method was based on the sector-field inductively coupled plasma mass spectrometry. Results indicated that Pd ions were rapidly eliminated from the body. The principal excretion was through the feces (650 ± 72.7 ng/g dry weight, at the Pd dose of 250 ng/mL), but at the higher dosing Pd was also eliminated through the urine (6.16 ± 1.91 ng/mL for the Pd intake of 250 ng/mL). A clear relationship between the Pd ingested dose and the Pd excretion amount was observed mainly in the feces. Absorbed Pd was mostly found in the kidney of rats (124.4 ± 23.0 ng/g dry weight, following the highest dose), while liver, lung, spleen and bones did not accumulate the metal. At the higher dosing, Pd content in the kidney raised proportionally with the Pd dose. Our findings may be useful to help in the understanding of the health impact of Pd dispersed in the environment as well as in identifying appropriate biological indices of Pd exposure.