說有80%肝癌患者驗出馬兜鈴酸基因
馬兜鈴酸 Aristolochic acid
因為馬兜鈴酸基因造成肝癌
所以或許這個資料有點幫助
DNA甲基化能關閉某些基因的活性,去甲基化則誘導了基因的重新活化和表達。
下調DNA甲基化的營養:
鎂、硒、維生素C、維生素D、兒茶素、花青素、薑黃素、茄紅素、蜂膠、大豆異黃酮
可是馬兜鈴酸在身體要怎麼代謝?
Aristolochic acid (AA)馬兜鈴酸(AA)
cytochrome P450 (CYP) 細胞色素P450
In human renal microsomes NADPH:CYP reductase is more effective in AA activation.
在人腎微粒體中,NADPH:CYP還原酶在AA激活中更有效。
Prostaglandin H synthase (cyclooxygenase, COX) is another enzyme activating AA in human renal microsomes.
前列腺素H合成酶(環加氧酶,COX)是人腎微粒體中另一種激活AA的酶。
Among the cytosolic reductases, NAD(P)H:quinone oxidoreductase (NQO1) is the most efficient
in the activation of AA in human liver and kidney.
在胞質還原酶中,NAD(P)H:醌氧化還原酶(NQO1)是人肝和腎中AA活化最有效的酶。
因此若能抑制NADPH:CYP還原酶、環加氧酶,COX、NAD(P)H:醌氧化還原酶(NQO1)
應該就能讓馬兜鈴酸不會產生毒性
進而代謝
CoQ10 reductases such as NADPH: quinone acceptor oxidoreductase 1 (NQO1)
CoQ10還原酶如NADPH:醌受體氧化還原酶1(NQO1)
Zn2+ was the most powerful inhibitor for NADPH-CoQ reductase
Zn2+(鋅離子)是NADPH-CoQ還原酶最強的抑製劑
IL-4 / IL-13顯著下調Cox-2的表達
能提高IL-4的元素:鋅、維生素A
Inhibitory effects of Cu(2+) on the cytochrome P450 (P450)-catalyzed reactions of liver microsomes
and reconstituted systems containing purified P450 and NADPH-P450 reductase (NPR) were seen.
觀察到Cu(銅2+)對肝微粒體和含有純化的P450和NADPH-P450還原酶(NPR)的重構系統的細胞色素P450(P450)催化反應的抑制作用。
However, Zn(2+), Mg(2+), Mn(2+), Ca(2+), and Co(2+) had no apparent effects on the activities of microsomal P450s.
然而,Zn(鋅上標2+),Mg(鎂上標2 +),Mn(錳上標2+),Ca(鈣上標2 +)和Co(鈷上標2 +)對微粒體P450活性沒有明顯影響。
Copper caused a decrease in semiquinone levels of NPR, although it did not disturb the rate of formation
of semiquinone.
銅導致NPR半醌含量下降,儘管它不影響半醌的形成速率。
Sensitive, Selective, and Irreversible Inhibition of Cyclooxygenase-2 (COX-2) Activity by Copper
銅對環氧合酶-2(COX-2)活性的敏感,選擇性和不可逆抑制
Cu2+ inhibited the constitutive and inducible expression of Nqo1 and Gst ya mRNAs in a time-dependent manner.
Cu2 +(銅離子)以時間依賴性方式抑制Nqo1的組成型和誘導型表達。
總結以上:
鋅、銅對於治療馬兜鈴酸造成的肝癌、協助馬兜鈴酸代謝應該都有幫助
建議可以多喝豆漿來治療肝的疾病
Vitamin C attenuates the toxic effect of aristolochic acid on renal tubular cells via decreasing
oxidative stress‑mediated cell death pathways.
維它命C通過降低氧化應激介導的細胞死亡途徑來減弱馬兜鈴酸對腎小管細胞的毒性作用。
因此維它命C可能在協助馬兜鈴酸代謝上也有幫助