Vitamin E co-treatment reduces Aroclor 1254-induced impairment of reproductive neuroendocrine function in Atlantic croaker.

Abstract:

:We have shown previously that exposure of Atlantic croaker to a PCB mixture (Aroclor 1254) results in impaired reproductive neuroendocrine function. In addition, we have identified hypothalamic tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin (5-hydroxytryptamine) synthesis, as a target of PCB neuroendocrine toxicity. In order to further elucidate the mechanisms of PCB neurotoxicity, the present study investigated whether PCB-induced decrease in hypothalamic TPH activity resulted from degradation of the enzyme protein. Fish were exposed to Aroclor 1254 in the diet (0.1 mg/100 g body weight (BW)/day) for 30 days. The PCB exposure elicited a significant decrease in hypothalamic TPH protein content, which could be at least partially responsible for the reduced TPH activity. To test whether a similar PCB exposure could cause oxidative damage in croaker hypothalamic tissues, we examined the formation of malondialdehyde (MDA) protein adducts as a marker of lipid peroxidation (LPO). The same dose of PCB increased the MDA-protein adduct formation in the hypothalamus. In a separate experiment, the role of vitamin E, an antioxidant, to prevent or decrease the effect of PCB on hypothalamic TPH activity and gonadal growth was examined. The vitamin E co-treatments (1 and 10 mg/100 g BW/day) with PCB significantly reduced the effects of PCB on TPH activity and gonadal growth. These results suggest possible involvement of oxidative processes in PCB neurotoxicity.

journal_name

Mar Environ Res

authors

Khan IA,Thomas P

doi

10.1016/j.marenvres.2004.03.077

keywords:

subject

Has Abstract

pub_date

2004-08-01 00:00:00

pages

333-6

issue

2-5

eissn

0141-1136

issn

1879-0291

pii

S0141-1136(04)00064-9

journal_volume

58

pub_type

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