However, it may have exerted its protective effect against APAP hepatotoxicity by either inhibiting the bio-activation of APAP or the inactivation of NAPQI reactive intermediate as it prevented drop of GSH levels. Inducing repair process in the liver cells may also be involved in the mechanism of hepatoprotection of tomato extract. Lipid peroxidation was also decreased by the extract which suggests prevention of free radical formation in the process of APAP toxicity.
ADN is a very potent antiarrhythmic drug, with almost ideal antiarrhythmic properties; however, its use is limited by the not infrequent and sometimes serious side effects. The mechanism of ADN toxicity is multifactorial and still uncertain. Adverse effects of ADN on the cell immune responses have been reported to be mediated by phospholipase inhibition or drug-induced oxidative stress and membrane destabilization (Massey et al., 1995). The pathogenesis of ADN-induced pulmonary toxicity is not well known. Our results showed a decrease in reduced GSH levels and a slight increase in lipid peroxidation after administration of ADN which suggests that an oxidative stress mechanism is involved in its pulmonary toxicity. Other researchers also have proposed an oxidant mechanism and showed that several antioxidants can reduce lysosomal phospholipidosis and prevent ADN toxicity (Ruch et al., 1991; Agoston et al., 2003). In this research, tomato extract rich in lycopene prevented GSH depletion and induction of lipid peroxidation and partially prevented tissue damage by ADN, which suggests an oxidative stress and free radical involvement, although it may not be the main mechanism of pulmonary toxicity of ADN. Cyclosporin A, a cyclic decapeptide of fungal origin, is the most widely used immunosuppressive drug in organ transplantation and in the treatment of autoimmune disorders. However, its clinical use has been hampered by frequent reports of its nephrotoxicity.
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然而，它也許施加了它的防護作用反對APAP hepatotoxicity通過或者禁止APAP的生物活化作用或NAPQI活性中間體的鈍化作用作為它的防止了GSH水平下落。 導致在肝细胞的修理過程在蕃茄萃取物的hepatoprotection機制也許也介入。 油脂過氧化由在APAP毒力過程中建議自由基形成預防的萃取物也減少。 ADN是一種非常有力抗節律不齊的藥物，與幾乎理想的抗節律不齊藥的物產 然而，它的用途由不少有和有時嚴肅的副作用限制。 ADN毒力機制是多因子的和不定。 ADN的不利影響對細胞免疫反應報告由磷脂酶禁止或藥物導致的氧化重音和膜不穩定。 ADN導致的肺毒力發病原理不是知名的。 我們的結果顯示了在減少的GSH水平的減退和在油脂過氧化的輕微的增量，在ADN的管理以後哪些建議一個氧化重音機制在它的肺毒力介入。 其他研究員也提出了氧化劑機制並且表示，幾抗氧劑可能減少lysosomal phospholipidosis和防止ADN毒力。 在這研究，蕃茄番茄紅素油脂過氧化和由ADN的部分地被防止的損傷的被防止的GSH取盡和歸納的萃取物富有，建議氧化重音和自由基介入，雖然它可能不是ADN肺毒力主要機制。 Cyclosporin A，一循環decapeptide黴菌起源，是最用途廣泛的免抑制疫力的藥物在器官移植和在自動免疫的混亂的治療。 然而，它的臨床用途由它的中毒性腎損害頻繁報告阻礙了。