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 Resjournal_title
Marine environmental researchauthors
Khan IA,Thomas Pdoi
10.1016/j.marenvres.2004.03.077keywords:
subject
Has Abstractpub_date
2004-08-01 00:00:00pages
333-6issue
2-5eissn
0141-1136issn
1879-0291pii
S0141-1136(04)00064-9journal_volume
58pub_type
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