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Forty-seven fish (24 endemic Alburnus tarichi, Güldenstädt, 1814; 8 Capoeta capoeta, Guldenstaedt, 1772; 15 mirror carp Cyprinus carpio, L., 1758) and 13 mussel (Unio stevenianus, Krynicki, 1837) samples, with 10 specimens per sample, were collected from Van Lake, Turkey, and rivers flowing into it. Gamma-HCH was detected in 21 Alburnus tarichi samples (56.57 ng/g ± 22.18 ng/g) and in two Capoeta capoeta samples (27.6 ng/g and 36.45 ng/g). Beta-HCH was detected in 8 Alburnus tarichi samples (24.95 ng/g ± 4.42 ng/g) and in two mussel samples (101.25 ng/g and 129.44 ng/g). HCB was found in one Alburnus tarichi sample (14.4 ng/g) and one mussel sample (181.25 ng/g). The compound 4,4'-DDE was detected in 21 Alburnus tarichi samples (87.13 ng/g ± 32.23 ng/g), in 9 mirror carp samples (304.82 ng/g ± 100.76 ng/g) and one mussel sample (149.31 ng/g). PCB 28 was detected in one Alburnus tarichi (19.46 ng/g) sample and PCB 101 was found in one Capoeta capoeta (60.16 ng/g) sample. PCB 118 was detected in one mirror carp sample (277.5 ng/g) and in two Capoeta capoeta samples (43.77 and 54.38 ng/g). PCB 128 was detected in only one Capoeta capoeta sample (141.48 ng/g). It is concluded that (i) efforts should be made to reduce contamination of aquatic environments by these compounds and that (ii) their levels in fishery products from Van Lake and connected streams should be monitored and publicly reported on a regular basis.

We investigated dose-related pathological alterations and apoptosis in rat kidney tissue exposed to permethrin. Histopathological findings, apoptotic cell death and urinary 3-phenoxybenzoic acid concentrations (3-PBA) were evaluated. Different doses of permethrin were administered to animals by oro-gastric gavage. A dose-dependent increase of urine 3-PBA concentration was observed in all the permethrin-treated groups. SDS-PAGE separated 30-45 kD and 100-220 kD protein bands in all experimental groups. Histopathologically, degenerative changes were observed in the epithelial lining of the S1, S2, and S3 segments of the renal proximal tubules. Apoptotic cells were seen in the inner stripe of the outer medulla in Group I, and both the cortex and medulla in Groups II and III. Immunohistochemical staining of caspase 3 and caspase 9 also was observed in the same areas. Our results suggest that damage to regions of the proximal tubules is dose-related, and caspase-9-dependent, mitochondria-related apoptotic cell death could play an important role in permethrin-induced nephrotoxicity. We also observed morphologically necrotic cells. We concluded that both necrosis and apoptosis are produced by permethrin.

The aim of this study was to evaluate dichlorvos toxicity in terms of nitro-oxidative stress by determining 3-nitrotyrosine (3-NT) levels in the fore, mid, and hindbrain regions in acutely exposed rats. Male SpragueDawley rats were randomly allocated to three groups of eight. Group 1 was administered a single intraperitoneal dichlorvos dose of 1.8 mg kg -1 (0.1xLD 50 ) and group 2 a dose of 9 mg kg -1 (0.5xLD 50 ). The control group received 0.5 mL saline solution via the same route. 3-NT and tyrosine (TYR) levels were measured using high performance liquid chromatography with a photodiode array detector (HPLC-PDA) and expressed as a ratio of 3-NT to TYR. The 3-NT/1000 TYR ratios increased significantly in the fore-, mid-and hindbrains of the exposed groups compared to control (p<0.01). In the forebrain, the increase was also significant between the treated groups. Our study has confirmed that acute exposure to dichlorvos leads to nitro-oxidative stress in the brain and that 3-NT may play a role in the mechanism of dichlorvos neurotoxicity.

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