One of the main purposes of this thesis was to establish and develop methods used for ESR spin trapping of superoxide and nitric oxide in our lab. The methods utilised were based upon protocols used by Reger (unpublished data) at the German Heart Center in Munich in order to investigate mechanisms proposed by Edin (unpublished work) for the sustained elimination of hyper radiosensitivity (HRS) in cultured cells. The measurements by Reger using a table top ESR spectrometer yielded inconclusive results and it was desirable to repeat these measurements using a larger, more involved ESR spectrometer which allows for more sensitive acquisition. Two main groups of ESR spin trapping experiments were conducted; superoxide/ROS in cells was measured with cyclic hydroxylamine spin probe 1-hydroxy-3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine (CMH) at ambient temperature, with measurements on both cell suspension and supernatant. Nitric oxide measurements were made with colloidal iron-dithiocarbamate spin trap Fe(II)(DETC)2 at 77 K. The ESR signal originating from the oxidised cyclic hydroxylamine spin probe CM• was detected in both cell suspensions and supernatant from cells incubated with CMH. The oxidising species was not decidedly identified. Molecular oxygen in the air was seen to give rise to a high background oxidation. No significant difference between ROS levels as measured in primed and unprimed T-47D and T98G cells was found. A series of experiments examining the level of oxidation of the spin probe with reoxygenation time after hypoxia were carried out using the supernatant protocol. A reproducible trend in which the ESR signal detected was seen to increase after 1 – 2 minutes to a plateau at around 5 – 8 minutes followed by a more or less clear decline. These results were taken to reflect the increase in ROS generation upon reoxygenation of cells after hypoxia. Colloidal iron-diethyldithiocarbamate spin trap Fe(II)(DETC)2 was employed to measure nitric oxide generated in cultured cells. The method was successfully applied to samples supplemented with an NO•-donor, and the characteristic spectrum for the NO•-Fe(II)(DETC)2 spin adduct was observed.Measurements of basal NO• proved more of a challenge and the characteristic NO•-Fe(II)(DETC)2 spectrum was not observed for any of the samples. The acquired spectra were largely dominated by a signal which was attributed to the Cu(II)(DETC)2 complex, which arises from chelation by free DETC of intracellular copper. One proposed reason for the absence of the NO•-Fe(II)(DETC)2 signal in the basal samples is that there is very little NO• produced in these cell, or that what little there is is preferentially scavenged by superoxide in the absence of functional superoxide dismutase (SOD). Another, and possibly coexistent reason, is that inadequate control of oxygen contamination occluded the signal. Since no conclusive signal from nitric oxide was detected in the cells, no conclusions concerning differences in nitric oxide production between primed and unprimed cells could be made on these grounds. These results contradict the results obtained by Reger, in which signals due to nitric oxide allegedly was measured. A signal of unknown origin was observed with varying intensity for most of the basal samples. This was speculated to originate from chelation of some intracellular transition metal other than copper by DETC, or contamination with some chemical used in cell culture or preparation of samples, possibly serum or phenol red.