Masako Hagihara

Lipid peroxide levels of serum lipoprotein fractions of diabetic patients

Abstract The elevation of lipid peroxide level has been considered as a cause of the degeneration of organs or tissues (1–6). It was also considered that the lipid peroxide formed in the primary site would be transferred via blood to other organs or tissues where the damage would be provoked by the propagation of lipid peroxidation (7,8). Recently, it was reported from our laboratory that plasma lipid peroxide levels of diabetic patients were significantly higher than those of control subjects and that the levels in diabetics with angiopathy were markedly higher than those in diabetics without angiopathy (9). From these results, we suspected that a high level of lipid peroxide in plasma would be, at least partly, the cause of angiopathy in patients suffering from diabetes, and that it would be worthwhile to obtain further information on the lipid peroxides of blood plasma of diabetic patients. The present paper deals with the lipid peroxide levels of serum lipoprotein fractions of diabetic patients examined in relation to some abnormal features of lipid metabolism.

Female sterility in mice lacking the basigin gene, which encodes a transmembrane glycoprotein belonging to the immunoglobulin superfamily

Basigin (Bsg) is a transmembrane glycoprotein belonging to the immunoglobulin superfamily. Bsg knock‐out mice exhibit infertility of both sexes. Based on limited results, defective implantation has been considered to be the cause of the female infertility. We demonstrate here that disruption of the Bsg gene produces the failure of female reproductive processes including not only implantation but also fertilization. Bsg mRNA expression in cumulus cells and basolateral localization of the Bsg protein in the endometrial epithelium further support the importance of Bsg in these processes.

Effect of thermal injury on lipid peroxide levels of rat

Abstract Since the report of Cannon and Bayliss (1) who believed that fluid loss from circulation was not sufficient to account for the circulatory failure commonly seen in battle casualties, occurrence of “toxic factor” has gathered much attention. In fact, in these cases fluid therapy is very successful in acute phase, but late death often occurs. Accordingly, many investigations on toxic factor after burn injury have been carried out. Among them, the following reports drew our attention. Allgower et al. (2) claimed to have identified the toxin as a lipid-protein polymer formed from a component of cell walls of the skin. Helmkamp et al. (3) found significant reduction in the levels of polyunsaturated fatty acids such as linoleate, arachidonate, and docosahexaenoate in red cell membrane phospholipid of severely burned humans. Loebl et al. (4) suggested that erythrocyte destruction in early postburn period would be due to a substance circulating in thermally injured patients. Rai and Courtemanche (5) described that with an increase in burn index, the fall in vitamin A level became greater. Sugiyama et al. (6) recently reported that extensive release of prostaglandins into the blister a few hours after burn injury would partly explain general symptoms of the burn syndrome. From these reports, we suspected that burn toxin might be similar to lipid peroxides. In the present study, therefore, the levels of lipid peroxides in animal tissues and serum of postburn period were measured.

Activities of dipeptidyl peptidase II, dipeptidyl peptidase IV, prolyl endopeptidase, and collagenase-like peptidase in synovial membrane from patients with rheumatoid arthritis and osteoarthritis.

We examined the activities of peptidases in the synovial membrane from patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Dipeptidyl peptidase II (DPP II), prolyl endopeptidase (PEP), and collagenase-like peptidase (CLP) activities were higher in knee joint synovial membrane from patients with RA than in that from patients with OA. DPP II and PEP activities in knee joint synovial membrane of patients with RA increased in parallel with the increase in joint fluid volume, whereas DPP IV activity decreased in parallel with the increase in joint fluid volume. These results suggest that these peptidases in the synovial membrane may play some role in immunological disturbances in the joints of patients with RA. Measurement of these peptidases in synovial membrane may be useful in the diagnosis of the severity of local joint inflammation.

Concentrations of neopterin and biopterin in the cerebrospinal fluid of patients with Parkinson's disease

The concentrations of neopterin and biopterin in CSF of 18 younger and 10 older, control patients and of 18 patients with Parkinsons disease were measured by high-performance liquid chromatography with fluorescence detection. Both neopterin concentrations and the neopterin to biopterin ratios in CSF were lower in 50-year or younger group than in 51-year or older group. Biopterin concentrations were also decreased but not significantly in the older group. The concentrations of neopterin and biopterin in CSF of patients with Parkinsons disease were lower than those of the age-matched older control group. However, the neopterin/biopterin ratios tended to be lower but not change significantly as compared to the age-matched older control group.

Post-proline cleaving enzyme in human cerebrospinal fluid from control patients and parkinsonian patients

PPCE activity was found in human CSF by using a HPLC-fluorescence method. PPCE activity in CSF from control patients without neurological diseases was 2.19 +/- 0.78 (mean +/- SD) pmole (hr)-1.(ml)-1. PPCE activity in CSF from patients with Parkinsons disease was significantly decreased while PPCE activity in serum did not change significantly.

Dipeptidyl-aminopeptidase II in human cerebrospinal fluid: changes in patients with Parkinson's disease

By using a sensitive and specific method, DAP II activity was found in CSF. DAP II activity in CSF of control patients without neurological diseases was 0.416 +/- 0.141 (mean +/- SD) nmole/min/ml and was higher than DAP IV activity in CSF, 0.221 +/- 0.062 (mean +/- SD) nmole/min/ml. In contrast, DAP II activity in serum was 1.16 +/- 0.16 (mean +/- SD) nmole/min/ml and was lower than serum DAP IV activity [41.85 +/- 3.36 (mean +/- SD) nmole/min/ml]. This relatively high activity of DAP II in CSF compared with the activity of DAP IV in CSF together with recent histochemical evidence on the localization of DAP II in some neurons (7) suggests that CSF DAP II may be derived from the brain and may be a marker of some peptidergic neurons. DAP II activity in CSF of patients with Parkinsons disease was significantly increased, whereas DAP IV activity in CSF did not change significantly.

Changes in membrane fluidity of erythrocytes during cell maturation.

Abstract The measurements of the fluorescence polarization of perylene embedded in erythrocyte membranes were carried out with normal and reticulocyte-rich blood, and the microviscosity of erythrocyte membranes was calculated from the polarization degree. In intact cells, reticulocyte membranes had a significantly lower microviscosity than normal erythrocyte membranes, while in ghosts no significant difference in membrane microviscosity was observed between reticulocytes and mature erythrocytes.

The relationship between collagen metabolism and temporomandibular joint osteoarthrosis in mice

The histologic changes in the temporo mandibular joint (TMJ) and the activity of serum collagenase-like (CL) peptidase and prolyl endopeptidase (PEP) were compared in mice with spontaneous osteoarthrosis (C57 black mouse/6 Silverberg (C57BL/6S) and control mice (C57 black mouse/6N (C57BL/6N) and ddY). The onset of osteoarthrosis of the TMJ in the C57BL/6S mice was noted at 12 weeks of age. Clefting in the chondrocyte layer was noted at 24 to 36 weeks of age; chondrocyte cluster and pannus at 36 to 60 weeks of age; and clefts deep in the bone and formation of osteophytes at 72 to 96 weeks of age. CL-peptidase and PEP activity significantly higher in C57BL/6S mice than in osteoarthrosis-free C57BL/6N and ddY mice. These changes occurred at an earlier age than the histologic changes. The findings suggest that these enzymes may play a significant role in the onset of osteoarthrosis in joints.

Cyclosporin A, an immune suppressor, enhanced neurotoxicity of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to mice

N-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) was systemically administrated into C57BL/6N mice for 8 days. Tyrosine hydroxylase activity and dopamine content in striatum and hypothalamus were reduced markedly, and the reduction was more manifest in the striatum. Cyclosporin A, an immune suppresser, enhanced the neurotoxicity of MPTP, when it was injected to mice in combination with MPTP. Tyrosine hydroxylase activity in the striatum was reduced to 109 +/- 20 from 350 +/- 46 pmol/min/mg protein of control, when mice were injected by MPTP alone. The enzyme activity was further reduced to 68.4 +/- 12.2 pmol/min/mg protein by injection of MPTP in combination to cyclosporin A. In addition, dopamine and biopterin contents in the striatum decreased quite in parallel to the reduction of tyrosine hydroxylase activity. On the other hand, cyclosporin A itself did not effect tyrosine hydroxylase activity and dopamine and biopterin contents in the striatum and hypothalamus. These data suggest cumulative effect of cyclosporin A to the neurotoxicity of MPTP.