A variety of compounds including drugs, carcinogens, steroids and fatty acids are metabolized by microsomal monooxygenase system in the liver. The effect of phenobarbital(PB) on the monooxygenase system in the liver microsomes of neonatal, immature- and adult-rats of both sexes were investigated. In the liver microsomes of rats, the activities of cytochrome P-450, NADPH-cytochrome C reductase, cytochrome b₅, NADH-cytochrome C reductase, p-nitroanisole-O-demethylase and the formation of lipid peroxide were assayed : the following results were obtained. 1) In the liver microsomes of rats, the activities of cytochrome P-450 and NADPH-cytochrome C redutase were increased in PB treated rats compared to control. Among the developmental stages, the contents of hepatic microsomal cytochrome P-450 and NADPH-cytochrome C reductase were highest in the female adult rat and the male immature rat. 2) The contents of hepatic microsomal cytochrome b₅ and NADH-cytochrome C reductase were increased in PB treated rats compared to control. Among the developmental stages the content of hepatic microsomal cytochrome b₅ was highest in the female adult rat and the male immature rat, whereas the content of hepatic microsomal NADH-cytochrome C reductase was highest in the adult rats of both sexes. 3) The formation of lipid peroxide was increased in PB treated rats compared to control. Among the developmental stages the formation of lipid peroxide was highest in the female adult rat and the male immature rat. 4) The activity of hepatic microsomal p-nitroanisole-O-demethylase was increased in PB treated rats compared to control. Among the developmental stages the activity of p-nitroanisole-O-demethylase was highest in the female adult rat and the male immature rat.

In cholestatic rats, effects of phenobarbital or cholic acid on hepatic microsomal cytochrome p-450 and b₅ were investigated. The total contents of both cytochrome p-450 and cytochrome b₅ were decreased after bile duct ligation and the administration of estradiol. When cholic acid or phenobarbital was adminstrated in cholestatic rats, the decrease of cytochrome p-450 was prevented. The effects of cholic acid or phenobarbital on both ring-hydroxylation and N-hydroxylation of AAF in cholestatic rat hepatic microsomal fraction were studied. N-hydroxylation of AAF in bile duct ligated rat liver microsomes was reduced by 34%, but ring-hydroxylation was increased by 51%. In estradiol administrated rat, both ring-hydroxylation and N-hydroxylation of AAD was increased by 20 to 25%. In cholic acid administration, both ring-hydroxylation and N-hydroxylation was increased by about 10%. N-hydroxylation of AAF in phenobarbital treated rats was reduced more than ring-hydroxylation was reduced compared to the bile duct ligated group. Estradiol treated group which administrated with cholic acid or phenobarbital exhibited inhibited effects of N-hydroxylation.

The levels of hepatic microsomal cytochrome P-450 in preimplantation rats were determined 1) The activities of the hepatic microsomal cytochrome P-450 associated with the events leading to implantation were gradually increased in preimplantation rats. 2) The level of the hepatic microsomal cytochrome P-450 was peak, 2.65 nmoles/mg protein, on day 4 in normal preimplantation rat. 3) The activity of the hepatic microsomal cytochrome P-450 was decreased in ovariectomized rat than normal rat. 4) The hepatic microsomal cytochrome P-450 level in ovariectomized rat was peak, 2.39 nmoles/mg protein, on day 5. 5) We observed the fact thar the activity of microsomal P-450 was delayed in ovariectomized rat. 6) We confirmed the fact that the hepatic microsomal cytochrome P-450 level was affected by steroid hormone.

This study was designed to determine and report the the protein contents in Korean industrial food eaten in our daily lives. Samples were industrial foods of cereals, legumes, meats, milk, fishes, shellfishes, vegetables, and fruits. The protein contents were determined by micro-kjeldahl method. 1) The content of protein was generally higher in the industrial foods than in the natual foods. 2) The contents of protein in the natural legumes were high compared with that of the industrial foods of meats, milk, fishes and shellfishes. 3) The amount of protein in the industrial foods of vegetables and fruits was very low compared with that of industrial foods of meats, milk, fishes and shellfishes.

Cytochrome P-450 is sometimes called the microsomal carbon monoxide-binding pigment. It is present in the microsomal fraction of several animal tissues, and also in the mitochondrial fraction of adrenal cortex, but not in the mitochondria of other tissues. Cytochrome P-450, the liver microsomal drugmetabolizing enzyme is membranebound and fraction as multicomponent electron transport system for the metabolism of a variety of endogenous substrates(such as steroids, fatty acids, and bile acids) and exogenous substance (such as drugs, carcinogens, insecticides, and many other foreign compounds). The effect estrous cycle and preimplantation on the levels of hepatic microsomal cytochrome P-450 in mice were determined. In effect of estrous cycle on microsomal cytochrome P-450 level, the most increment was at estrus. The content of cytochrome P-450 was increased significantly at pregnant Day 3 of preimplantation.

Cytochrome P-450 is a terminal oxidase of the hepatic microsomal monooxygenase system associated with the oxidative biotransformation of a varity of lipophilic endogenous and exogenous compounds, and generally is assayed by CO-binding spectro-photometry of dithionite-reduced samples. In well fed normal male rats with or without stress condition, the dffect of antiulcer drug; cimetidine, sulpiride and diazepam on the level of microsomal cytochrome P-450 were determined. Only stress condition produced on significant effect in cytochrome P-450 contents. Administration of cimetidine, sulpiride and diazepam in this condition caused a 44.1%~87.5% increment in cytochrome P-450, diazepam produced the most increase. After diazepam treatment of rats, the peak position of cytochrome P-450 shifted to a longer wave length of 452 nm.

A large number of chemicals have the ability to induce cancer in a variety of tissues of various hosts, including man. Despite current interest in the viral etiology of a limited number of specific human cancers, it is generally believed that most human cancers may be caused by chemicals present either as environmental contaminants or produced in certain instances from endogenous factors. Although great advances have been made in studies of the metabolism of many chemical carcinogens and on mechanisms of their reaction with cellular constituents the fact stands out that we do not understand the pathobiological action of single chemical carcinogen. It has been known for along time that many classes of chemical carcinogens become covalantly bound to DNA. RNA, and proteins of the cells in target tissues. It has become axiomatic that the induction of cancer by chemical carcinogens results from such covalent binding to one or more of these cellular macromolecules. However, despite much intensive reserch, the macromolecular target has not yet unequivocally been identified. Among the important classes of chemical carcinogens that become covalently bound to tissue macromolecules are polycyclic aromatic hydrocarbons(PAH), aromatic amines, nitrosamines, and aflatoxins. These carcinogens must be matabolized to a chemically reactive form which then reacts to form covalent macromolecular complexes. The millers and others have discovered that these metabolic actvations are carried out primarily by the microsomal mixed function oxidases. These enzyme systems, which are usually considered detoxifying and drug metabolizing, are the same ones that activate chemicals to carcinogenic and mutagenic forms.