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中文提要: 本篇論文首度以酵素動力學的觀點來探討重金屬鎘對吳郭魚
（Oreochromis mossambicus） 仔魚吸收鈣離子速率的影響。將吳郭魚
仔魚以20 mg/l的鎘處理4小時後，仔魚吸收鈣離子 的速率即會明顯的
下降。當比較剛孵化及孵化後第3天仔魚吸收鈣離子速率受影響的程度時
發現，鎘抑制其吸收鈣離子速率的程度分別為其對照組（未以鎘處理之同
齡仔魚）的32﹪ 及45﹪。此外，鈣離子流速測定顯示剛孵化及孵化後
第3天仔魚對鈣離子的親和力 （Km的倒數）分別降低為同齡對照組
的1/19.3及1/17.4，說明了這種抑制作用是一種 競爭性的抑制作用(
competitive inhibition)。在另一個實驗中，以20 mg/l的鎘浸泡 剛孵
化及孵化後第3天的吳郭魚仔魚，比較當牠們體內累積等量的鎘時，相對
於未以鎘處理 之同齡仔魚吸收鈣離子的速率，發現此時孵化後第3天的
仔魚吸收鈣離子的速率受鎘的影響 較大。雖然牠們吸收鈣離子的速率
在20 mg/l的鎘浸泡處理下，在24小時內皆能迅速恢復到 對照組的水準
，但是當檢測牠們體內鈣含量的變化時，卻只有孵化後第3天的仔魚體鈣
總含 量會因為鎘的處理而遠低於對照組，由此可推知相對於剛孵化的仔
魚，3天大的仔魚對鎘是 比較敏感的。由孵化後的吳郭魚仔魚中發現，
隨著發育，牠體內的鈣含量、鈣離子吸收速率 及其極限初速(Vmax）在
第3天有驟升現象，配合鰓的增生分化及功能逐漸健全，可推知鈣 離子
的充分吸收對維持仔魚正常發育的重要性。然而，因為鎘與鈣都是經由相
同的孔道被 吸收，增加對鈣離子的吸收效率，勢必也提高了仔魚吸收鎘
的機會，如果在此發育的關鍵 時刻，因為受到鎘的作用，而使得牠對鈣
離子的吸收受到抑制，無法得到成長所需的鈣離子， 進而導致低鈣血症
（hypocalcemia）等病變，則是造成孵化後第3天的吳郭魚仔魚對鎘較為
敏感的原因。如果預將剛孵化的吳郭魚仔魚浸泡在20 mg/l的鎘環境中3天
後，發現此時鎘 對仔魚吸收鈣離子速率的競爭性抑制作用已不復存在；
相反的，相較於對照組的仔魚，由 鈣離子吸收速率及其極限初速的測量
，發現有前處理的吳郭魚仔魚不但表現出對鈣離子有 較高的吸收速率，
而且如果以50 mg/l的鎘前處理剛孵化的仔魚3天後，則可提高牠對鎘的
耐受能力達10倍以上。最後，在這馴化過程中，吳郭魚仔魚表現出的驚人
適應能力，其中 的可能機制，在論文中也有探討。
英文提要: The present study for the first time discussed the
toxic effects of Cd2+ on the Ca2+ influx kinetics in the
developing tilapia (Oreochromis mossambicus) larvae. External
20 mg/l Cd2+ competitively inhibited the Ca2+ uptake within 4
hours and resulted in a great increase of Km values for Ca2+
influx in the 0-day-old larvae and the 3-day-old larvae (19.3
and 17.4 folds) as compared with their respective controls.
Consequently, the actual Ca2+ influx rates in larvae at 0.2 mM
Ca2+ were suppressed by 32-45 %. In another experiment, the
3-day-old larvae were more sensitive to Cd2+ than the 0-day-
old larvae when they accumulated the same amount of Cd2+
internally. Although the Ca2+ influx rates in the 0- and 3-day-
old larvae could restore to the levels of their respective
control within 24 hours after transferring to 20 mg/l Cd2+,
total body calcium content was significantly reduced only in
the 3-day-old larvae. On the other hand, the development of
gills, together with increasing Ca2+ uptake efficiency, is
important for obtaining sufficient Ca2+ for normal growth.
However, Cd2+ and Ca2+ share a common uptake pathway in
freshwater fishes, rapid increase in Ca2+ influx rate after
hatching would also lead to higher Cd2+ uptake. A drop in body
calcium content by Cd2+ exposure will lead to a retardation in
larval growth. Therefore, I conclude that if Ca2+ uptake was
interfered at this critical stage of development, the body
calcium in the developing larvae could not get back to its
normal level resulting in a hypocalcemia. Furthermore, tilapia
larvae pre-exposed to 20 mg/l Cd2+ for 3 days were subjected
to both 0 and 20 mg/l Cd2+ for a 4-hour Ca2+ influx test. The
Ca2+ influx rate was not inhibited by internal or external Cd2+
and a enhanced Ca2+ uptake ability could be found in these
Cd2+-adapted larvae. Furthermore, a ten-fold increase in 96-h
LC50 has been found in the tilapia larvae pre-exposed to 50 mg/l
Cd2+ for 3 days in comparison with the naive 3-day-old larvae
in the same water chemistry. Some possible adaptation
mechanisms involved in the increased metal-tolerance in the
course of exposure has been discussed.
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