Integrating enzymatic responses to organic chemical exposure with total oxyradical absorbing capacity and dna damage in the european eel Anguilla anguilla

Environmental Toxicology and Chemistry - Tập 22 Số 9 - Trang 2120-2129 - 2003
Francesco Regoli1, Gary W. Winston2, Stefania Gorbi1, Giada Frenzilli3, Marco Nigro3, Ilaria Corsi4, Silvano Focardi4
1Istituto di Biologia e Genetica, Universita' Politecnica delle Marche, 60100 Ancona, Italy
2Ministry of Health, Department of Environmental Health, Jerusalem, Israel
3Dipartimento di Morfologia Umana e Biologia Applicata, Università di Pisa, Pisa, Italy
4Dipartimento di Scienze Ambientali, Università di Siena, Siena, Italy

Tóm tắt

AbstractIn this work, susceptibility to oxidative stress was analyzed under laboratory conditions in the European eel Anguilla anguilla. Eels were treated with increasing concentrations of benchmark environmental pollutants, namely, benzo[a]pyrene ([BaP], at 0, 0.1, 1, 10, and 50 mg/kg), β‐naphthoflavone ([BNF], at 0, 0.1, 1, 10, and 50 mg/kg), Arochlor® 1254 (at 0, 0.1, 1, 10, and 50 mg/kg), and 2,3,7,8‐tetrachlorodibenzo p‐dioxin ([TCDD], at 0, 0.01, 0.1, 1, and 2 μg/kg). The integral relationships were analyzed between induction of ethoxyresorufin O‐deethylase (EROD) activity, its involvement in perturbing oxyradical metabolism, and the role of cytochrome P450 and/or oxidative stress in mediating genotoxic effects. To reveal whether the oxidative status in exposed organisms was altered as a result of chemical exposure, measurements of the main endogenous antioxidant defenses were integrated with the measurement of total oxyradical scavenging capacity (TOSC) toward peroxyl radicals and hydroxyl radicals (·OH). This approach permits discriminating the resistance of a tissue toward different forms of oxyradicals, thereby indicating a differential role for specific reactive oxygen species (ROS) in perturbing the balance between prooxidant and antioxidant mechanisms. All the analyzed chemicals promoted EROD induction (reflective of CYP1A) and altered either the levels or the activities of the antioxidants studied, which might be anticipated to exert alterations in oxyradical metabolism. Analysis of TOSC suggested the prevalence of metabolic oxidative pathways leading to the more reactive ·OH on exposure to the chemicals studied. Of these chemicals, enhanced EROD activity correlated with genotoxic damage only in the cases of the nonhalogenated hydrocarbons BaP and BNF. The highest degree of genotoxic damage was consistently observed in organisms in which the capacity to absorb or scavenge ·OH was lowest. These data suggests a general relationship between oxidative stress and loss of DNA integrity in juvenile eels exposed to the chemicals studied herein.

Từ khóa


Tài liệu tham khảo

10.2307/3430851

Livingstone DR, 1996, Environmental Xenobiotics, 143

10.1016/S0025-326X(01)00060-1

10.1016/S0166-445X(00)00141-7

Di Giulio RT, 1995, Fundamentals of Aquatic Toxicology, Effects, Environmental Fate, and Risk Assessment, 523

10.1016/S0891-5849(99)00203-8

10.1016/S0166-445X(00)00091-6

10.1016/S0166-445X(00)00159-4

10.1016/0141-1136(93)90021-Q

Weinberg RA, 1989, Oncogenes, antioncogenes and the molecular bases of multistep carcinogenesis, Cancer Res, 49, 3713

10.1016/0141-1136(94)00003-8

10.1006/eesa.1997.1585

10.1016/S0166-445X(99)00061-2

10.1016/S0166-445X(00)00087-4

10.1016/S0025-326X(01)00141-2

10.1016/S0025-326X(02)00120-0

10.1016/S0891-5849(97)00277-3

10.1006/taap.1999.8637

10.1016/0014-4827(88)90265-0

10.1016/0921-8777(95)00063-1

10.1016/0166-445X(96)00002-1

10.1016/S0166-445X(96)00802-8

10.1016/S0045-6535(00)00500-2

10.1016/S0048-9697(01)00759-8

10.1016/S0141-1136(01)00113-1

10.1016/S0166-445X(00)00086-2

10.1016/S0160-4120(00)00101-X

Hahn ME, 1998, Mechanisms of innate and acquired resistance to dioxin‐like compounds, Rev Toxicol, 2, 395

10.1016/S0166-445X(99)00043-0

10.1016/0141-1136(93)90052-2

10.1289/ehp.8771105

10.3109/03602539308993984

10.1016/S0166-445X(96)00819-3

10.1006/eesa.1998.1675

10.1016/S0166-445X(99)00082-X

10.1016/0166-445X(94)00064-W

10.1016/S0166-445X(97)00059-3

10.1016/S0048-9697(99)00484-2

Halliwell B, 1999, Free Radicals in Biology and Medicine

10.3109/10409239309086794

10.1016/S1532-0456(02)00129-1

10.1016/0166-445X(94)90020-5

10.1016/S0141-1136(97)00118-9

10.1515/CCLM.2003.003