The purpose of the study was to investigate an effect of water temperature on a non-specific immune response and mortality of tilapia, Oreochromis niloticus, following a bacterial infection. Seventy five tilapia acclimated to 25℃ were then transferred at 16 and 36℃, and examined for non-specific immune responses over 12-96 h. Respiratory burst activity was reduced significantly in the group of fish cultured at 16 and 36℃ over 24-96 h, whereas phagocytic activity decreased significantly in the group of fish reared at a low temperature (16℃) over 12 and 24 h and high temperatures (36℃) over 12-96 h. Lysozyme activity diminished significantly in the group of fish transferred to 16℃ over 12-48 h, but increased significantly in the group of fish at 36℃ over 48 and 96 h. Alternative complement pathway (ACH50) decreased significantly when transferred to 16℃ after 12 h, but increased significantly when transferred to 36℃ after 24 h. In a challenging test, 30 tilapia reared at 25℃ were injected intraperitoneally with Streptococcus iniae at a dose of 2x107 cfu/fish, and then reared onward at water temperatures of 15, 25 (control), and 36℃. Over 12-96 h, the cumulative mortality of S. iniae-injected fish held in 16 and 36℃ was significantly higher than that of injected-fish held in 25℃ In conclusion, transfer of tilapia from 25℃ to low temperature (16℃) after 12 h, and transfer of fish from 25℃ to high temperature (35℃) reduced their immune capability. Furthermore, tilapia under temperature stress at 16 and 36℃ from 25℃ decreased its resistance against S. iniae

Although the vegetable Angelica keiskei (AK) has widely been utilized for the purpose of general health improvement among Korean population, its functionalities are not very well defined. In this study, we examined the effects of methanol extract of AK in rats on the biochemical changes induced by two hepatotoxins, D-galactosamine (GalN) and carbon tetrachloride ( CCl₄). AK was orally administered once daily for 7 days to male rats at 200and 500 mg/kg, before hepatotoxins. Effects of AK were assessed 24 hr later. AK pretreatments at 200 and 500 mg/kg significantly blunted GalN-induced elevation in liver lipid peroxidation, plasma aspartate-transaminase (AST) and alanine-transaminase (ALT) activities. AK also prevented, after 500 mg/kg but not after 200 mg/kg, the GalN-induced elevation in triglyceride, total cholesterol and LDL-cholesterol levels. Differently from against GalN-induced toxicity,AK did further elevate the CCl₄-induced rise in AST, ALT and lipid peroxidation. These results suggest that AK, when pre-administered prior to GalN, exerted protective effects against GalN-induced hepatotoxicity, in contrast however,AK exacerbated that induced by CCl₄. To explore possible mechanism for the toxicity-potentiating effects of AK on CCl₄, the activity of hepatic drug metabolism after AK treatment was assessed. It was observed that AK increased the activity of aniline hydroxaylase, a cytochrome P450 isoenzyme responsible for metabolic activation of CCl₄. This finding suggests that hepatoprotective effects of AK are not equally expected depending on hepatotoxins employed.