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* * * * ★★★肽聚糖是细胞壁主要成份,凡能破坏肽聚糖结构、或抑制其合成的物质都能使细胞壁损伤,甚至杀死细菌。———溶菌酶、青霉素】 溶菌酶(lysozyme):可切断NAM的G1和NAG的C4之间?—1,4的糖苷键,破坏肽聚糖支架,引起细菌裂解。(所以又称乙酰胞壁质酶。 ) 对Gˉ菌,在EDTA存在下,受溶菌酶作用。 溶菌酶处理后的菌细胞应保存在弱高渗(0.1 ~0.2M)蔗糖液中。 * 青霉素对细菌细胞壁的作用点不同于溶菌酶,因此对细菌细胞的影响亦不尽相同。 Penicillin: the story of an antibiotic The antibacterial effect of penicillin was discovered by Alexander Fleming in 1929. He noted that a fungal colony had grown as a contaminant on an agar plate streaked with the bacterium Staphylococcus aureus, and that the bacterial colonies around the fungus were transparent, because their cells were lysing. Fleming had devoted much of his career to finding methods for treating wound infections, and immediately recognised the importance of a fungal metabolite that might be used to control bacteria. The substance was named penicillin, because the fungal contaminant was identified as Penicillium notatum. Fleming found that it was effective against many Gram positive bacteria in laboratory conditions, and he even used locally applied, crude preparations of this substance, from culture filtrates, to control eye infections. However, he could not purify this compound because of its instability, and it was not until the period of the Second World War (1939-1945) that two other British scientists, Florey and Chain, working in the USA, managed to produce the antibiotic on an industrial scale for widespread use. All three scientists shared the Nobel Prize for this work, and rightly so - penicillin rapidly became the wonder drug which saved literally millions of lives. It is still a front line antibiotic, in common use for some bacterial infections although the development of penicillin-resistance in several pathogenic bacteria now limits its effectiveness (see later). * ★ 肽聚糖是细胞壁的主要成份,凡能破坏肽聚糖结构或抑制其合成的物质都能使菌细胞壁缺损。 ★★大多数细菌细胞壁缺损后后,因不能耐受菌体内部的高渗透压而裂解死亡。 ★★ 用溶菌酶处理置于等渗溶液中的G+菌,可以得到细胞壁几乎可以完全被脱去,对渗透压敏感的原生质体; → → 用溶菌酶处理G-菌时必须有螯合剂——乙二胺四乙酸的存在,而且只能到除去部分细胞壁,带有部分残留细胞壁的菌细胞称为球形体。 ★★★L-form细菌是在某些环境条件下所形成
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