A. Adam et al., NITROFURANTOIN-INDUCED HEPATIC AND PULMONARY BIOCHEMICAL-CHANGES IN MICE FED DIFFERENT VITAMIN-E DOSES, Pharmacology & toxicology, 79(6), 1996, pp. 334-339
The hepatic and pulmonary effects of nitrofurantoin (40 mg/kg, intrape
ritoneally) were determined at 4 and 24 hr following its administratio
n in mice fed for 10 weeks with a vitamin E sufficient, deficient or e
nriched diet. Liver glutathione (GSH) was reduced by nitrofurantoin at
4 hr but was unchanged 20 hr later. Nitrofurantoin did not affect liv
er glutathione peroxidase, glutathione reductase or superoxide dismuta
se activities. Liver catalase activities were decreased by nitrofurant
oin at 4 hr. Lung GSH levels were increased whilst glutathione peroxid
ase activity was decreased at 4 and 24 hr. Lung glutathione reductase
activity was reduced in certain groups. Nitrofurantoin did not affect
lung superoxide dismutase, but catalase was decreased at 24 hr. Liver
malondialdehyde levels were increased by nitrofurantoin in the vitamin
E deficient group whilst lung malondialdehyde levels remained unchang
ed. Both liver and lung malondialdehyde levels were unaffected by vita
min E supplementation when compared to the vitamin E-sufficient group
These results suggest that nitrofurantoin (40 mg/kg) was deleterious t
o the liver and lung. Nitrofurantoin-induced lipid peroxidation was se
en in vitamin E deficiency but an increase in dietary vitamin E conten
t did not provide additional protection compared to the recommended da
ily allowance. The antioxidant acitivities of alpha-tocopherol and gam
ma-enriched tocotrienol were similar.