Kageaki Aibara

Lipofuscin and lipofuscin-like substances

Lipofuscin is defined as being a yellowish brown, lipid-rich, heterogeneous, cytoplasmic granular pigment emitting an intense yellow autofluorescence when excited with ultraviolet light, which accumulates in various tissues of animals during their aging. It is believed that the pigments are derived from the reaction of some of reactive secondary products including malonaldehyde, formed during membranous lipid peroxidation, with amino groups of phospholipids and proteins, etc., and that these formations are accompanied by alteration of the membrane structure and inactivation of the enzymes. The fluorescence measurement of the pigments is widely used as a parameter of lipid peroxidation in vivo as well as in vitro. However, their origin, chemical structure, biological significance or fate has not as yet been fully elucidated. This article introduces and discusses the recent studies on these problems.

Immunopotentiative effect of polysaccharide from kefir, grain, KGF-C, administered orally in mice

Since a water-soluble polysaccharide (KGF-C) from the kefir grains was shown to have the property of retarding tumor growth in vivo when administered orally, the effect of KGF-C was examined on antibody responses to thymus-dependent antigen, sheep red blood cells (SRBC), and thymus-independent antigen, dinitrophenyl-Ficoll and trinitrophenyl-lipopolysaccharide. Antibody response in mice intubated with KGF-C was enhanced to low doses of SRBC, but not to optimal or high doses. The optimal dose of KGF-C required for the enhancement was 100 mg/kg body weight. The time-course studies on KGF-C administration implied that KGF-C exerted its effect on the early events of anti-SRBC response. The enhancement was not due to the alteration of kinetics of anti-SRBC responses. Furthermore, the enhancing effect on antibody responses to thymus-independent antigens, such as dinitrophenyl-Ficoll and trinitrophenyl-lipopolysaccharide, was observed neither in nu/nu nor in nu/+ mice, and the effect on delayed-type hypersensitivity response to a low dose of SRBC in normal mice was also found. These findings suggest that the oral immune enhancement by KGF-C is elucidated probably through T-cell but not through B-cell participation.

Elevation of thiobarbituric acid values in the rat liver intoxicated by T-2 toxin

In the present study we first demonstrated that T-2 toxin markedly stimulated lipid peroxidation specifically in the liver of rats. The amount of lipid peroxides in the liver, estimated by the thiobarbituric acid (TBA) method, increased dose dependently, being proportional to the extent of its acute toxicity measured by various parameters in rats fed a commercial diet. Further, to elucidate the mechanism of lipid peroxidation and its role in hepatic injury caused by T-2 toxin, time-course studies on the correlation between lipid peroxide content and some biological and histopathological data were undertaken in rats given 4 mg of the toxin/kg perorally. The TBA reactive substances in the liver began to increase after 6 hr. However, much earlier than this there were some other alterations, which included decreases in the amount of cytochrome P-450 in the liver, of GPT (thereafter an increase) and phospholipids in the plasma, and of basophilic masses in the hepatocytes (arrayed as a rough endoplasmic reticulum in the electron micrograph). The vitamin E-deficient study showed that vitamin E markedly inhibited the stimulative effect of T-2 toxin on lipid peroxidation, but not diminish any other measured parameters of the injury. The toxin-induced stimulation of lipid peroxidation does not appear to be caused by activation of microsomal NADPH-cytochrome c reductase nor by a decrease in the level of cytosolic glutathione peroxidase. These results suggest that T-2 toxin might induce some alteration of the membrane structure and consequently might stimulate lipid peroxidation in situ.

Interactions of aflatoxin B1 and blood components of various species in vitro: Interconversion of aflatoxin B1 and aflatoxicol in the blood

The fate of aflatoxin B1 (AFB1) in the blood of various species of animals was studied in vitro. Examination of the distribution of radioactivity in blood incubated with [14C]AFB1 at 37 degrees C showed that high levels of radioactivity were associated with blood cells. The radioactivity was readily removed from the blood cells by washing with fresh plasma, indicating loose binding of AFB1 to blood cells. Most of the radioactivity in plasma was bound to protein. These results suggest that a large part of the AFB1 in blood in vivo may be carried not only by the plasma proteins but also by the blood cells. When chloroform extracts of plasma of [14C]AFB1-treated mouse, rat, duckling, and hamster blood were developed by thin-layer chromatography, high levels of radioactivity were found in both the AFB1 region and the aflatoxicol (AFL) region. Incubation of blood with nonradioactive AFB1 and AFL showed marked interconversion of AFB1 and AFL in the blood of rats, hamsters, mice, and Mongolian gerbils, but not in the blood of guinea pigs, rhesus monkeys, squirrel monkeys, or humans. Interconversion occurred in red blood cell suspensions but not in plasma, indicating that the red blood cells are responsible for AFB1-AFL interconversion in the blood.