Abstract

Several markers of hydrocarbon exposure and sublethal effects were measured in rainbow surfperch Hypsurus caryi and rubberlip surfperch Rachochilus toxodes from a shallow natural petroleum seep and from reference areas in the Santa Barbara Channel. Hydrocarbon exposure was assessed by an HPLC-based analysis of fluorescing compounds in the bile. Compounds fluorescing at wavelengths of naphthalene were significantly elevated in bile of rainbow surfperch (~3×), but not rubberlip surfperch, from the seep. Compounds fluorescing at wavelengths of phenanthrene were significantly elevated in bile of both species (~2× to 3×) relative to those from the comparison areas. Content of cytochrome 4501A (CYP1A) in hepatic microsomes of both species from the petroleum seep was significantly greater than in individuals from the reference areas (~10× in rainbow surfperch and ~2× in rubberlip surfperch). Immunohistochemical analysis also showed greater content of CYP1A in both species from the petroleum seep. The CYP1A content of gill epithelia in particular was greatly different between fish from the seep and reference areas. A variety of histopathological lesions were documented in gills, livers and kidneys of both species. Total lesion scores were not different between the two groups of rubberlip surfperch. However, in the rainbow surfperch total lesion scores from petroleum seep fish were approximately twice as high in gills and one and one-half times as high in liver as those from the comparison area. In the latter species liver lesions were relatively mild, but in gills relatively severe lesions occurred, including cartilage dysplasia, abnormal branching and fusion of lamellae, various sorts of inflammation, aneurysms, and epithelial hyperplasia. Such interspecific differences in hydrocarbon exposure and response are consistent with the greater reliance on benthic feeding and more limited movements of the rainbow surfperch. It is suggested that cartilage displaysia and abnormal branching of gill filaments and lamellae are biological markers for xenobiotic compounds that induce CYP1A.

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