Gusarov Ivan, Shatalin Konstantin, Starodubtseva Marina, Nudler Evgeny
Department of Biochemistry, New York University School of Medicine, 550 First Avenue, New York, NY 10016, USA.
Science. 2009 Sep 11;325(5946):1380-4. doi: 10.1126/science.1175439.
Bacterial nitric oxide synthases (bNOS) are present in many Gram-positive species and have been demonstrated to synthesize NO from arginine in vitro and in vivo. However, the physiological role of bNOS remains largely unknown. We show that NO generated by bNOS increases the resistance of bacteria to a broad spectrum of antibiotics, enabling the bacteria to survive and share habitats with antibiotic-producing microorganisms. NO-mediated resistance is achieved through both the chemical modification of toxic compounds and the alleviation of the oxidative stress imposed by many antibiotics. Our results suggest that the inhibition of NOS activity may increase the effectiveness of antimicrobial therapy.
细菌一氧化氮合酶(bNOS)存在于许多革兰氏阳性菌中,已证实在体外和体内均可从精氨酸合成一氧化氮。然而,bNOS的生理作用在很大程度上仍不清楚。我们发现,bNOS产生的一氧化氮可增强细菌对多种抗生素的抗性,使细菌能够存活并与产生抗生素的微生物共享生存环境。一氧化氮介导的抗性是通过对有毒化合物的化学修饰以及减轻许多抗生素所施加的氧化应激来实现的。我们的结果表明,抑制一氧化氮合酶的活性可能会提高抗菌治疗的效果。