Despite a close interaction between cadmium (Cd) and long-chain polyunsaturated fatty acid (LC-PUFA) metabolism, the influence of Cd exposure on the endogenous synthesis of LC-PUFA has received little attention. In the present study, we hypothesized that Cd exposure would affect the synthesis of LC-PUFA in the marine fish silver pomfret (Pampus argenteus). Therefore, the molecular basis of LC-PUFA biosynthesis and regulation was investigated as the first step to understanding the mechanisms underpinning the effects of Cd exposure. Thereafter, transcriptional regulation of the genes that participate in LC-PUFA biosynthesis and regulation by Cd exposure were also explored. Our results showed that fatty acyl desaturase 2 (Fads2) and elongases of very long-chain fatty acids 5 (Elovl5), two key enzymes involved in LC-PUFA biosynthesis, enabled silver pomfret to biosynthesize 20:3n–6 and 20:4n–3 from 18:2n-6 and 18:3n-3. The results also raise the possibility that silver pomfret may have the ability to produce docosahexaenoic acid (DHA, 22:6n-3) from endogenous eicosapentaenoic acid (EPA, 20:5n-3). The expression of silver pomfret fads2 and elovl5 was transcriptionally regulated by the peroxisome proliferator activated receptor α (Pparα). The expression of fads2, elovl5 and pparα in the brain was significantly increased in response to Cd exposure. In addition, Cd exposure significantly reduced the DHA concentration and significantly increased the malondialdehyde concentration in the brain of silver pomfret. Cd exposure likely increases brain-specific DHA synthesis from EPA by transcriptionally activating fads2 and elovl5 via Pparα in silver pomfret. This regulation may be a coping mechanism for the reduction of DHA caused by Cd-oxidative stress in the brains of silver pomfret.

尽管镉（Cd）和长链多不饱和脂肪酸（LC-PUFA）代谢之间存在紧密的相互作用，但镉暴露对LC-PUFA内源性合成的影响很少受到关注。在本研究中，我们假设Cd暴露会影响海水鱼类银po鱼（Pampus argenteus）中LC-PUFA的合成）。因此，研究LC-PUFA生物合成和调控的分子基础是了解了解镉暴露影响机理的第一步。此后，还探讨了参与LC-PUFA生物合成的基因的转录调控和Cd暴露调控。我们的结果表明，脂肪酰基去饱和酶2（Fads2）和超长链脂肪酸5的延长酶（Elovl5）是LC-PUFA生物合成中涉及的两个关键酶，使po鱼能够生物合成20：3n–6和20：4n– 3从18：2n-6和18：3n-3。结果还增加了po鱼可能具有从内源二十碳五烯酸（EPA，20：5n-3）产生二十二碳六烯酸（DHA，22：6n-3）的能力。银po fads2和elovl5的表达被过氧化物酶体增殖物激活的受体α（Pparα）转录调控。响应于Cd暴露，大脑中fads2，elovl5和pparα的表达显着增加。此外，镉的暴露显着降低了po鱼脑中的DHA浓度，并显着提高了丙二醛在大脑中的丙二醛浓度。镉暴露可能通过m鱼中的Pparα转录激活fads2和elovl5，从而增加了EPA引起的大脑特异性DHA的合成。这种调节可能是减少po鱼脑中Cd氧化应激引起的DHA减少的应对机制。