Nitric oxide participates in many physiological functions, includmg vasodilation, inhibition of platelet aggregation, neurotransmission and immune regulation [3]. NO is formed from the amino acid arginine by NO synthase (NOS) with stoichiometric generation of citrulline [4]. However, since NO formation under hypoxia is not blockable by NOS inlubitors, the efiiciency of NOS may be greatly reduced under hypoxic umditions [5]. We suggest that XO is a possible alternative source of NO under hypoxic conditions. HXO was purified from breast milk as detailed previously [6]. All experiments were performed in a Microflow Mkl anaerobic cabinet (MDH, Hampshire). Reactions were performed in 5Oml sealed flasks in the presmce of 0.1 jtM HXO and 1.0 mM NADH and various concmtrations of nitrite (Figure 1) with total volume of Iml solution. The formation of NO, rep- as parts per billion (ppb), was directly quantified with a thermal energy analyzer (TEA-502, Thermo Electron Cop.) which specifically deteds* N= O by chemilumineSenCe following reaction with ome to produce nitrogen dioxide in an excited state; relaxation ofthis molecule to the ground state is aocompanied by emission of a characteristic energy in the near-infrared region of the spedm.

Under hypoxic conditions, NO is generated by HXO in the presence of nitrite and NADH at pH 7.4. NO generation as a function of nitrite concentration for a solution containing 0.1 pM HXO and 1.0 mM NADH is shown (Figure 1). However, NO generation is not detedable in the absace of HXO. The &ect of the XO inhibitor,