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Impact of exposure to metals on gene...

Sorrentino, Claudio.

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Impact of exposure to metals on gene expression induced by aromatic hydrocarbons and its ecotoxicological implications.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Impact of exposure to metals on gene expression induced by aromatic hydrocarbons and its ecotoxicological implications./
Author:	Sorrentino, Claudio.
Description:	242 p.
Notes:	Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1290.
Contained By:	Dissertation Abstracts International65-03B.
Subject:	Health Sciences, Toxicology. -
Online resource:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3127498
ISBN:	0496747624

Impact of exposure to metals on gene expression induced by aromatic hydrocarbons and its ecotoxicological implications.
Sorrentino, Claudio.

Impact of exposure to metals on gene expression induced by aromatic hydrocarbons and its ecotoxicological implications. - 242 p.

Source: Dissertation Abstracts International, Volume: 65-03, Section: B, page: 1290.

Thesis (Ph.D.)--New York University, 2004.

Metals and aromatic hydrocarbons (AHs) often co-occur in aquatic ecosystems. Consequently, beginning in their earliest life-stages, fish are often co-exposed to mixtures of these pollutants throughout their lives. Although the effects of individual metals and AHs have been widely investigated, little is known about the effects of co-exposure. My hypothesis is that metals can modulate some of the biological activities of AHs in fish. If this hypothesis is true, then the presence of metals in the Hudson River (HR) may contribute to the resistance to PCBs and dioxins previously demonstrated in its Atlantic tomcod (Microgadus tomcod) population. In acutely exposed adult tomcod, cadmium, nickel, or chromium, and in part arsenic inhibited benzo[a]pyrene-(B[a]P) or PCB77-induced hepatic cytochrome P4501A1 (CYP1A1) mRNA expression. The acute effects of chromium on CYP1A1 transcription in adults were confirmed at the protein level. In chronically co-exposed larvae, chromium superinduced B[a]P-stimulated CYP1A1 transcription, but decreased CYP1A protein expression, indicating that modulation occurred at both levels independently. HR larvae were more sensitive to chromium than larvae from the cleaner Miramichi River (MR). This increased sensitivity could be interpreted as a biological cost of resistance to AHs in HR fish. B[a]P caused high mortality in MR, but not HR embryos, indicating that HR tomcod are resistant also to polycyclic AHs (PAHs). Co-exposure to chromium decreased B[a]P-induced mortality. Both AHs accelerated the time to hatch. Co-exposure to chromium or arsenic partially inhibited the shortening of the time to hatch, whereas zinc had the opposite effect. Metals did not alter the teratogenic effects of AHs. B[a]P uptake and binding to DNA were lower in HR than in MR embryos and larvae. In MR embryos, co-exposure to chromium inhibited B[a]P uptake. B[a]P binding to DNA also was inhibited by low concentrations of chromium (0.1 and 1 ppm), but 10 ppm chromium had the opposite effect. In conclusion, co-exposure to metals modulated some, but not all, of the effects of exposure to AHs at different levels. The presence of metals in the ecosystem may help to explain the resistance of the HR Atlantic tomcod population to the biological effects of exposure to AHs.

ISBN: 0496747624Subjects--Topical Terms:

1017752
Health Sciences, Toxicology.

Impact of exposure to metals on gene expression induced by aromatic hydrocarbons and its ecotoxicological implications.
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500 $a Adviser: Isaac I. Wirgin.
502 $a Thesis (Ph.D.)--New York University, 2004.
520 $a Metals and aromatic hydrocarbons (AHs) often co-occur in aquatic ecosystems. Consequently, beginning in their earliest life-stages, fish are often co-exposed to mixtures of these pollutants throughout their lives. Although the effects of individual metals and AHs have been widely investigated, little is known about the effects of co-exposure. My hypothesis is that metals can modulate some of the biological activities of AHs in fish. If this hypothesis is true, then the presence of metals in the Hudson River (HR) may contribute to the resistance to PCBs and dioxins previously demonstrated in its Atlantic tomcod (Microgadus tomcod) population. In acutely exposed adult tomcod, cadmium, nickel, or chromium, and in part arsenic inhibited benzo[a]pyrene-(B[a]P) or PCB77-induced hepatic cytochrome P4501A1 (CYP1A1) mRNA expression. The acute effects of chromium on CYP1A1 transcription in adults were confirmed at the protein level. In chronically co-exposed larvae, chromium superinduced B[a]P-stimulated CYP1A1 transcription, but decreased CYP1A protein expression, indicating that modulation occurred at both levels independently. HR larvae were more sensitive to chromium than larvae from the cleaner Miramichi River (MR). This increased sensitivity could be interpreted as a biological cost of resistance to AHs in HR fish. B[a]P caused high mortality in MR, but not HR embryos, indicating that HR tomcod are resistant also to polycyclic AHs (PAHs). Co-exposure to chromium decreased B[a]P-induced mortality. Both AHs accelerated the time to hatch. Co-exposure to chromium or arsenic partially inhibited the shortening of the time to hatch, whereas zinc had the opposite effect. Metals did not alter the teratogenic effects of AHs. B[a]P uptake and binding to DNA were lower in HR than in MR embryos and larvae. In MR embryos, co-exposure to chromium inhibited B[a]P uptake. B[a]P binding to DNA also was inhibited by low concentrations of chromium (0.1 and 1 ppm), but 10 ppm chromium had the opposite effect. In conclusion, co-exposure to metals modulated some, but not all, of the effects of exposure to AHs at different levels. The presence of metals in the ecosystem may help to explain the resistance of the HR Atlantic tomcod population to the biological effects of exposure to AHs.
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