Hepatotoxicity of herbicide Sencor in goldfish may result from induction of mild oxidative stress.

The effects of 96 h exposure to 7.14, 35.7, or 71.4 mg L(-1) of Sencor were studied on liver and plasma parameters in goldfish, Carassius auratus L. Goldfish exposure to 71.4 mg L(-1) of Sencor for 96 h resulted in a decrease in glucose concentrations in plasma and liver by 55%, but did not affect liver glycogen levels. An increase in the activity of aspartate aminotransferase, alanine aminotransferase and lactate dehydrogenase (by 24-27%, 32-72%, and 87-102%, respectively) occurred in plasma of Sencor exposed goldfish, whereas in liver activities of these enzymes decreased (by 15-17%, 19%, and 20%, respectively). Lactate concentration in plasma increased by 22-36% in all treated fish groups, whereas in liver it increased by 64% only after exposure to 35.7 mg L(-1) of Sencor. Herbicide exposure enhanced lipid peroxide levels by 49-75% and decreased activities of catalase by 46%, glutathione reductase by 25-48% and glutathione peroxidase by 21-26% suggesting development of oxidative stress in liver. The treatment induced various histological changes in goldfish liver, such as dilated sinusoids, hypertrophy and dystrophy of hepatic cells and detachment of endothelial cytoplasm with diffuse hemorrhage. The data collectively let us propose that mild oxidative stress might be responsible for the hepatotoxicity of Sencor.

Histopathological and biochemical changes in goldfish kidney due to exposure to the herbicide Sencor may be related to induction of oxidative stress.

Molecular mechanisms of toxicity by the metribuzin-containing herbicide Sencor to living organisms, particularly fish, have not yet been extensively investigated. In the present work, we studied the effects of 96 h exposure to 7.14, 35.7, or 71.4 mg L(-1) of Sencor (corresponding to 5, 25, or 50 mg L(-1) of its herbicidal component metribuzin) on goldfish (Carassius auratus L.), examining the histology, levels of oxidative stress markers, and activities of antioxidant and related enzymes in kidney as well as hematological parameters and leukocyte profiles in blood. The treatment induced various histopathological changes in goldfish kidney, such as hypertrophy of intertubular hematopoietic tissue, small and multiple hemorrhages, glomerular shrinkage, a decrease in space between glomerulus and Bowman's capsule, degeneration and necrosis of the tubular epithelium. Sencor exposure also decreased activities of selected enzymes in kidney; activities of catalase decreased by 31-34%, glutathione peroxidase by 14-33%, glutathione reductase by 17-25%, and acetylcholinesterase by 31%. However, glucose-6-phosphate dehydrogenase and lactate dehydrogenase activities increased by 25-30% and 22% in kidney after treatment with 7.14 or 35.7 mg L(-1) and 71.4 mg L(-1) Sencor, respectively. Kidney levels of protein carbonyls increased by 177% after exposure to 35.7 mg L(-1) of Sencor indicating extensive damage to proteins. Lipid peroxide concentrations also increased by 25% after exposure to 7.14 mg L(-1) of Sencor, but levels were reduced by 42% in the 71.4 mg L(-1) exposure group. The data indicate that induction of oxidative stress is one of the mechanisms responsible for Sencor toxicity to fish.

Assessment of both environmental cytotoxicity and trace metal pollution using Populus simonii Carr. as a bioindicator.

The level of environmental pollution in the city of Ivano-Frankivsk (Western Ukraine) has been assessed by means of roadside poplar trees as bioindicators. Dividable apical meristem cells of rudimentary leaves were quantitatively analysed for mitotic activity and distribution. Anaphases were further examined for chromosomal aberrations. Male catkins were also examined for sterile pollens. Accumulation of trace elements in vegetative buds was also evaluated in order to reveal source(s) of environmental pollution. Poplar trees growing in the urban environment proved to have increased chromosomal aberrations (up to 4-fold) and increased pollen sterility (up to 4-fold) as well as decreased mitotic activity (by factor 1.5) as compared to control sampling site. The biomarker data correlate moderately with increased (up to 4-fold) concentrations of Ni, Zn, Pb, Cd and Cu in vegetative tissues suggesting that probable cause of the environmental cytotoxicity may be vehicle emissions. The maximum increase in chromosomal aberrations (7-fold) and the minimum mitotic activity (half of the control one) were recorded in poplar trees growing in industrial suburb in vicinity of large cement production plant. Taking in mind insignificant bioaccumulation of trace elements in the industrial suburb, the high environmental toxicity has been ascribed to contamination in cement and asbestos particulates.