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Biomedical subjects

K Ohkawa

Publications and source records attributed to K Ohkawa.

At least 19 recordsLinked to original sources
PubMed2000

Depletion of protein kinase C (PKC) by 12-O-tetradecanoylphorbol-13-acetate (TPA) enhances platinum drug sensitivity in human ovarian carcinoma cells.

Down-regulation of protein kinase C (PKC) by 12-Otetradecanoylphorbol-13-acetate (TPA) enhances the sensitivity of human ovarian carcinoma 2008 cells to various types of platinum compounds such as cisplatin (DDP), carboplatin and (-)-(R)-2-aminomethylpyrrolidine (1,1-cyclobutanedicarboxylato)-platinum(II) monohydrate (DWA) by a factor of two- to threefold. TPA enhanced the sensitivity of the DDP-resistant 2008/C13*5.25 subline to each of these three drugs to the same extent as for the 2008 cells. The extent of PKC down-regulation and drug sensitization depended on the duration of TPA exposure; maximum effect was achieved with a 48 h pretreatment. Sensitization was TPA concentration-dependent and was maximal at 0.05 microM TPA. 2008 cells expressed only the PKCalpha and PKCzeta isoforms. Western blot analysis revealed that whereas the expression of PKCalpha was reduced by TPA the level of PKCzeta was not affected. These results suggest that PKCalpha is the isotype responsive to TPA in these cells and that platinum drug sensitivity can be modulated by this isoform alone. In parallel to its effect on PKCalpha, TPA decreased cellular glutathione content by 30 +/- 3 (standard deviation (s.d.) % in 2008 cells and by 41 +/- 3 (s.d.) % in 2008/C13*5.25 cells. TPA also increased accumulation of DDP and DWA by 70%, although this effect was limited to the 2008/C13*5.25 cells. TPA rendered 2008 and 2008/C13*5.25 cells resistant to cadmium chloride by a factor of 3.7 and 3.6-fold respectively, suggesting a significant increase in cellular metallothionein content. Although the mechanism of TPA induced sensitization is not yet fully understood, this study points to a central role for PKCalpha in modulating platinum drug sensitivity.

Antineoplastic Agents↗
PubMed2000

Identification of multiple transcription factors, HLF, FTF, and E4BP4, controlling hepatitis B virus enhancer II.

Hepatitis B virus (HBV) enhancer II (EnII) is a hepatotropic cis element which is responsible for the hepatocyte-specific gene expression of HBV. Multiple transcription factors have been demonstrated to interact with this region. In this study, the region from HBV nucleotides (nt) 1640 to 1663 in EnII was demonstrated to be essential for enhancer activity and to be another target sequence of putative transcription factors. To elucidate the factors which bind to this region, we used a yeast one-hybrid screening system and cloned three transcription factors, HLF, FTF, and E4BP4, from a human adult liver cDNA library. All of these factors had binding affinity to the sequence from nt 1640 to 1663. Investigation of the effects of these factors on transcriptional regulation revealed that HLF and FTF had stimulatory activity on nt 1640 to 1663, whereas E4BP4 had a suppressing effect. FTF coordinately activated both 3. 5-kb RNA and 2.4/2.1-kb RNA transcription in a transient transfection assay with an HBV expression vector. HLF, however, activated only 3.5-kb RNA transcription, and in primer extension analysis, HLF strongly stimulated the synthesis of pregenome RNA compared to precore RNA. Thus, FTF stimulated the activity of the second enhancer, while HLF stimulated the activity of the core upstream regulatory sequence, which affects only the core promoter, and had a dominant effect on the pregenome RNA synthesis.

Base Sequence↗
PubMed1999

Structural studies on sugar chains of carbohydrate-deficient transferrin from patients with alcoholic liver disease using lectin affinity electrophoresis.

It is well-known that microheterogeneity of human serum transferrin observed in alcoholics manifests as sialic acid-deficient transferrin isoforms, otherwise known as carbohydrate-deficient transferrin (CDT). A recent study demonstrated that serum CDT lacked one or both of the entire carbohydrate chains but the investigation required several troublesome procedures. The aim of the present study was to confirm the sugar chain structures of serum transferrin, and of serum CDT in particular, from patients with alcoholic liver disease (ALD) using conventional lectin affinity electrophoresis which might be useful in the clinical setting. The serum CDT obtained from ALD-patients was partially purified using an anion exchanger. Serum transferrin and the partially purified serum CDT were investigated by concanavalin A (Con A)- and Datura stramonium agglutinin (DSA)-affinity electrophoresis followed by antibody-affinity blotting and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) with Western blotting. By Con A-affinity electrophoresis, serum CDT was separated into weakly reactive and nonreactive transferrins which showed slower electrophoretic mobilities than those from the healthy controls. Moreover, nearly all of the serum CDT was nonreactive with DSA. On SDS-PAGE, the molecular masses of serum CDT were estimated to be approximately 75 and 72 kDa, which corresponded to those of partially and completely deglycosylated transferrin obtained from the healthy controls (78 kDa), respectively. In conclusion, these results indicated that the sugar chain structures of serum CDT from patients with ALD show not merely a loss of terminal sialic acids, but also the absence of asparagine-N-linked oligosaccharides.

Antibody Affinity↗
PubMed1999

Hypercholesterolemia and glomerular diseases in urinary screening of school children.

Although hypercholesterolemia frequently accompanies nephrotic syndrome, high serum total cholesterol (TC) levels are occasionally seen in children with non-nephrotic glomerular diseases. However, little is known of the significance, if any, of these elevated serum TC levels in non-nephrotic glomerular diseases. During the past 5 years, a total of 256,179 school children received yearly urinary screening at school for renal diseases and 1,702 children (0.66% of the total, although 174 children dropped out) had proteinuria and/or hematuria. Using the data obtained from the 1,528 children, we studied whether there is any association between serum TC levels and the presence of glomerular diseases. The detection rate of glomerular diseases (IgA nephropathy, membranoproliferative glomerulonephritis, focal segmental glomerular sclerosis, etc.) in the subjects with high serum TC levels (> or =200 mg/dl) was significantly higher (16 of 161, 9.94%, P<0.001) than in those with normal serum TC levels (<200 mg/dl) (10 of 1,367, 0.73%). There were no significant differences in serum albumin and blood urea nitrogen levels between the two groups. We conclude that children with chance proteinuria and/or hematuria may be at higher risk for glomerulonephritis of various types when they have unexplained hypercholesterolemia, and that measurement of serum cholesterol levels may be useful in urinary screening for renal diseases.

Adolescent↗
PubMed1999

Involvement of transporter associated with antigen processing 2 (TAP2) gene polymorphisms in hepatitis C virus infection.

BACKGROUND & AIMS: Transporter associated with antigen processing (TAP) has essential roles in the antigen-presenting systems, translocating antigenic peptides from the cytosol into the endoplasmic reticulum. The aim of this study was to clarify whether TAP polymorphisms are involved in hepatitis C virus (HCV) infection. METHODS: The 145 HCV-infected Japanese patients examined in this study were categorized into two groups: 36 carriers with persistently normal alanine transaminase (ALT) values and 109 patients with chronic liver disease (CLD). TAP2 gene phenotypes were determined by means of polymerase chain reaction-restriction fragment length polymorphism, and their frequencies were compared between the two groups. RESULTS: Frequencies of TAP2*0101, *0102, and *0201 were not different between the two groups. However, TAP2*0103 frequency in carriers with normal ALT levels was significantly higher than that in patients with CLD (44% vs. 16%; P = 0.00064, Pc < 0.005). Although the TAP2*0103 allele was tightly linked with class II DRB1*1302-DQB1*0604 haplotype in this study, the TAP2*0103 frequency in the normal ALT group was also significantly higher than that in the CLD group even in DRB1*1302-DQB1*0604-negative patients (31% vs. 10%; P = 0.0076, Pc < 0.05). CONCLUSIONS: These findings suggest that TAP2*0103 may be closely associated with low serum ALT activity in HCV-infected Japanese patients.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

Caspase-3 activation during apoptosis caused by glutathione-doxorubicin conjugate.

Glutathione-doxorubicin (GSH-DXR) effectively induced apoptosis in rat hepatoma cells (AH66) at a lower concentration than DXR. After 24 h of drug treatment, DNA fragmentation of the cells was observed at the concentration of 1.0 microM DXR or 0.01 microM GSH-DXR. Increase in caspase-3 activity and DNA fragmentation were observed within 12 h and 15 h after treatment with either drug. Intracellular caspase-3 activity was increased in a dose-dependent manner after treatment with DXR or GSH-DXR, and caspase-3 activity correlated well with the ability to induce DNA fragmentation. When the cells were treated with either DXR or GSH-DXR for only 6 h, apoptotic DNA degradation and caspase-3 activation occurred 24 h after treatment. DNA fragmentation caused by these drugs was prevented completely by simultaneous treatment with the caspase-3 inhibitor, acetyl-Asp-Glu-Val-Asp-aldehyde (DEVD-CHO), at 10 microM. By contrast, DNA fragmentation was not prevented by the caspase-1 inhibitor, acetyl-Tyr-Val-Ala-Asp-aldehyde (YVAD-CHO), at the same concentration as DEVD-CHO, and caspase-1 was not activated at all by the treatment of AH66 cells with both DXR and GSH-DXR. These results demonstrate that DXR and GSH-DXR induce apoptotic DNA fragmentation via caspase-3 activation, but not via caspase-1 activation, and that GSH-DXR enhances the activation of caspase-3 approximately 100-fold more than DXR. Moreover, the findings suggested that an upstream apoptotic signal that can activate caspase-3 is induced within 6 h by treating AH66 cells with the drug.

Animals↗
PubMed1999

Immunohistochemical and ultrastructural analysis of dysplastic epithelium of human ocular surface: basement membrane and intermediate filament.

PURPOSE: The dysplastic corneal epithelium is characterized by the abnormal proliferation of epithelial cells. The phenotypes of these cells have not been elucidated. We investigated whether such epithelium expresses the phenotypes of corneal or conjunctival epithelial cells. METHODS: The corneas and conjunctivae from four normal subjects and from one patient with epithelial dysplasia of the central cornea were immunostained for IV and VII collagens and for cytokeratins. Monoclonal antibodies against collagen IV reacted to the [alpha1(IV)]2alpha2(IV) or alpha5(IV) molecule. Anti-cytokeratin antibodies were used to define epithelial cell types. The ultrastructure of the basement membrane (BM) of each specimen also was examined. RESULTS: Type VII collagen immunoreactivity was detected in all the specimens of epithelial BM. The anti-collagen IV [alpha1(IV)]2alpha2(IV) antibody labeled the conjunctival BMs, not the BMs of the corneal epithelia, of each subject. The normal corneal epithelial BM, not the BM of the conjunctival or dysplastic corneal epithelium, was immunolabeled with anti-alpha5(IV) antibody. The pattern of cytokeratin expression in the corneal epithelial dysplasia resembled that seen in the normal conjunctivae. Small breaks in the BM of dysplastic corneal epithelium were ultrastructurally revealed. The number of hemidesmosomes in the dysplastic corneal epithelium was decreased as compared with that in the normal BM. CONCLUSION: The composition of collagen types within the BM and the cellular phenotype of the dysplastic epithelium in the cornea resembled those of conjunctival epithelium, not of the cornea.

Adult↗
PubMed1999

Serum ubiquitin levels in patients with alcoholic liver disease.

Serum concentrations of free ubiquitin and multiubiquitin chain as determined by immunoassays were compared between 10 healthy subjects, and 11 patients with alcoholic hepatic fibrosis, 10 with alcoholic cirrhosis, and 6 with viral liver cirrhosis. All measurements of multiubiquitin chains were expressed in terms of a standard multiubiquitin chain reference preparation 1. Serum concentrations (mean +/- SD) of free ubiquitin and multiubiquitin chains were significantly higher in patients with alcoholic cirrhosis (63.5 +/- 33.7 ng/ml and 7.5 +/- 4.6 ng/ml) than in the normal subjects (29.6 +/- 6.6 ng/ml, p < 0.05 and 4.1 +/- 1.7 ng/ml, p < 0.05), and those with alcoholic hepatic fibrosis (34.8 +/- 16.3 ng/ml, p < 0.05 and 3.0 +/- 0.7 ng/ml, p < 0.05) and viral liver cirrhosis (28.8 +/- 7.5 ng/ml, p < 0.05 and 4.2 +/- 1.3 ng/ml, p < 0.05). Serum levels of both forms of ubiquitin in six patients with alcoholic cirrhosis showed a tendency to decline after 3 months of abstinence. In a total of 14 patients with alcoholic liver damage, 11 with brain atrophy had significantly higher serum levels of both ubiquitin forms than did three patients without brain atrophy (p < 0.05). No correlation was seen between serum concentrations of either form of ubiquitin and liver function test results in the patients with alcoholic liver damage. However, serum levels of both forms of ubiquitin levels correlated significantly with cumulative alcohol intake (p < 0.05). A significant correlation (p < 0.05) also was observed between serum levels of multiubiquitin chains and mean corpuscular volume, a marker of alcohol consumption. These results suggest that the serum concentrations of ubiquitin, especially multiubiquitin chain is a good marker for the diagnosis of alcoholic cirrhosis.

Adult↗
PubMed1999

Identification of protein kinase B (PKB) as a phosphatidylinositol 3,4,5-trisphosphate binding protein in Dictyostelium discoideum.

We have searched for phosphatidylinositol (PI)-3,4,5-trisphosphate (PIP3) binding proteins in Dictyostelium discoideum using beads bearing a PIP3 analogue, PIP3-APB. One of the binding proteins with a molecular mass of 55 kDa was purified and its amino acid sequence was partially analyzed. Database searches showed that the analyzed sequence was identical to that of protein kinase B (PKB) of D. discoideum. The specific activity of D. discoideum PKB, when expressed together with constitutively active PI-3 kinase in mammalian cells, was elevated by about three-fold, suggesting that PKB could also act downstream of PI-3 kinase in Dictyostelium cells.

Amino Acid Sequence↗
PubMed1999

Calpain inhibitor causes accumulation of ubiquitinated P-glycoprotein at the cell surface: possible role of calpain in P-glycoprotein turnover.

P-glycoprotein (Pgp) is a plasma-membrane glycoprotein that confers multi-drug resistance (MDR) on cells and displays ATP-driven drug pumping. The possible contribution of calpain-mediated proteolytic pathways to the functional regulation of the Pgp molecule was evaluated using K562/DXR, MDR cells. N-Acetyl-L-leucyl-L-leucyl-norleucinal was effluxed by Pgp, but N-benzyloxycarbonyl-L-leucyl-L-leucinal (zLLal), an inhibitor of calpain, retarded the degradation of Pgp leading to accumulation of the molecule largely at the cell surface membrane. Treatment with brefeldin A did not obstruct the zLLal-induced Pgp accumulation. NH4Cl increased the cytoplasmic Pgp level, with a slight to significant decrease at the cell surface membrane. Ubiquitin-ELISA and western blot analysis confirmed that the Pgp molecule, which accumulated mainly at the cell surface, was ubiquitinated. However, lactacystin did not show any accumulation of Pgp in either the cytoplasm or the cell surface membrane, suggesting that the proteasome did not participate in the phenomenon. Additionally, the Pgp was limitedly proteolyzed by calpain into two 98 kDa and 69 kDa, fragments within one minute. Despite the increased accumulation of Pgp at the cell surface after treatment with calpain inhibitor, the cytoplasmic doxorubicin level of the cells treated with a calpain inhibitor was higher than that of non-treated cells and approached that of parental cells. These results indicated that calpain involved Pgp turnover and that calpain inhibition induced ubiquitinated Pgp-accumulation mainly at the cell surface membrane with a reduction in its own functions suggesting that the modulation of Pgp-turnover involves MDR-reversal by another approach.

ATP Binding Cassette Transporter, Subfamily B↗
PubMed1998

Subretinal administration of tissue-type plasminogen activator to speed the drainage of subretinal hemorrhage.

BACKGROUND: Bleeding into the subretinal space in the vicinity of the macula is associated with age-related macular degeneration or retinal arterial macroaneurysm. The prognosis for restoration of vision is poor in the presence of blood clots. METHODS: Using a simple device composed of three disposable syringes we injected tissue-type plasminogen activator (tPA) into the subretinal space during conventional vitrectomy in six patients to assist the draining of subretinal clots. RESULTS: Four of six patients recovered their visual acuity postoperatively, while visual acuity in the other patients was stabilized. CONCLUSION: Early drainage of subretinal hemorrhage assisted by the introduction of tPA into the subretinal space led to uncomplicated surgery and favorable postoperative results.

Aged↗
PubMed1998

Biodegradation of ornithine-containing polylysine hydrogels.

The degradation of the cross-linked cationic poly(amino acid)-glutaraldehyde (GA) hydrogels by two kinds of proteolytic enzymes, trypsin and Aspergillus Protease Type XXIII, and by seven species of soil filamentous fungi has been investigated using homo- and copolypeptides of lysine (Lys) and ornithine (Orn). Trypsin degraded the hydrogels prepared from poly(Lys) and copoly(Lys Orn)s but not poly(Orn), while Aspergillus protease degraded all of them. Degradation time of hydrogels by the two proteases became longer with increasing Orn content in the gel. Seven species of soil filamentous fungi were cultured with hydrogels on Czapeck medium to evaluate the degree of microbial degradation of the hydrogels, and the three species of the fungi, Aspergillus oryzae, Penicillium citrinum and Curvularia sp., were grown in culture with an accompanying degradation of the gel matrix, while the other four species, Mucor sp., Rhizopus sp., Cladosporium sp., and Trichoderma sp., were not. The degree of degradation of gel matrix with growth of the three fungi became lower with increasing Orn content in the gel matrix. The results might offer some clues to the applications for the controlled biodegradation of cationic poly(amino acid) hydrogel by introduction of Orn, suggesting that unnatural amino acid resists hydrolysis by proteases or microorganisms.

Aspergillus oryzae↗
PubMed1998

Effects of theophylline on lymphocyte phosphodiesterase activity.

1. To clarify part of the bronchodilating effects of theophylline, lymphocyte cyclic AMP (cAMP) and phosphodiesterase (PDE) activity in asthmatic patients and healthy adults were measured. 2. No clear differences in lymphocyte PDE activity were found regarding sexes, ages or the types of asthma. 3. Lymphocyte PDE activity in the asthma group was significantly higher than that in the control group. 4. Lymphocyte cAMP significantly increased at 30 and 60 min after intravenous injection of aminophylline in the asthma group. 5. Lymphocyte PDE activity significantly decreased 60 min after intravenous injection of aminophylline in the asthma group.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1998

Degenerated lens epithelial cells in rabbit and human eyes after intraocular lens implantation.

PURPOSE: To evaluate the role of lens epithelial cells (LECs) in posterior capsule opacification. SETTING: Departments of Ophthalmology and Pathology, Wakayama Medical College, Department of Anatomy, Kansai Shinkyu College, and Department of Ophthalmology, Kobe Kaisei Hospital, Japan. METHODS: We examined the presence of degenerated LECs on the capsules of the eyes of rabbits and a patient after intraocular lens (IOL) implantation. Phacoextraction of a crystalline lens and IOL implantation were done in 5 albino rabbits under general anesthesia. The animals were killed after 2 months. Lens capsules were removed and fixed. During vitreous surgery, a lens capsule with an IOL was removed from a patient. Ultrathin sections of specimens were studied by transmission electron microscopy. RESULTS: Presumed LECs proliferated between the posterior capsule and the IOL in association with collagenous matrix. Debris from the degenerated cells and destroyed intracellular organelles was also seen. CONCLUSION: Lens epithelial cells proliferating on the posterior capsule cannot survive indefinitely.

Aged↗
PubMed1998

Proteasome inhibitors which induce neurite outgrowth from PC12h cells cause different subcellular accumulations of multi-ubiquitin chains.

The effects of two proteasome inhibitors on neurite outgrowth from PC12h cells were investigated in terms of the mean length of the neurites and the frequency of occurrence of cells with long neurites. Benzyloxycarbonyl-leucyl-leucyl-leucinal (ZLLLal) and benzyloxycarbonyl-isoleucyl-t-butyl-glutamyl-leucinal (PSI) caused a significant elongation of PC12h cell neurites. Since ZLLLal is known to inhibit both calpain and proteasome activity, we examined the effects ofbenzyloxycarbonyl-leucyl-leucinal (ZLLal) which inhibits calpain activity to the same degree as ZLLLal, but which inhibits proteasome activity only weakly. ZLLal did not induce the significant elongation of neurites at any of the concentrations we studied. These results show that the inhibition of proteasome activity causes neurite elongation. We also quantified subcellular levels of multi-ubiquitin chains and free ubiquitin after treatments with PSI, ZLLLal and ZLLal. Treatment with ZLLal had no effects on levels of water- and urea-soluble multi-ubiquitin chains or of free ubiquitin either in the nucleus or in the cytoplasm. PSI and ZLLLal induced a large accumulation of water- and urea-soluble multi-ubiquitin chains and free ubiquitin in the nucleus. Similarly, PSI and ZLLLal increased cytoplasmic levels of urea-soluble multi-ubiquitin chains. On the contrary, PSI and ZLLLal had no effect on levels of water-soluble multi-ubiquitin chains or free ubiquitin in the cytoplasm. This is the first study to demonstrate subcellular differences in the accumulation of multi-ubiquitin chains and free ubiquitin during the neurite elongation induced by proteasome inhibitors.

Animals↗
PubMed1998

Role of GABA receptors in the bronchial response: studies in sensitized guinea-pigs.

BACKGROUND: Gamma-aminobutyric acid (GABA), an important inhibitory neurotransmitter in the mammalian central nervous system, is also found in peripheral tissues, including the lung. GABA has recently been shown to modulate the contraction of airway smooth muscle. OBJECTIVE: We studied the effect of GABA on the contractile properties of tracheal smooth muscle by measuring the tension of the trachea isolated from non-sensitized and ovalbumin (OA)-sensitized guinea-pigs under isometric conditions. METHODS: Guinea-pigs were sensitized by intraperitoneal doses of OA to prepare a bronchial asthma model. Tracheal spiral rings were prepared from the OA-sensitized as well as normal, non-sensitized guinea-pigs. Using the tracheal preparations, the effects of GABA and GABAa and GABAb receptor agonists (muscimol and baclofen) and antagonists (bicuculline and saclofen) on the basal tone of the trachea and on tracheal contraction induced by electrical field stimulation (EFS) were determined. The effect of GABA on tracheal contraction induced by exogenous acetylcholine was also studied. RESULTS: GABA and GABA agonists and antagonists had no effect on the basal tone of normal guinea-pig tracheae. Both GABAa and GABAb receptor agonists, as well as GABA, suppressed EFS-induced contraction of normal guinea-pig tracheae in a reversible, dose-dependent manner. Moreover, this suppression was reserved to the control level by either GABAa and GABAb receptor antagonists. In tracheal spiral ring prepared from OA-sensitized guinea-pigs, GABA and baclofen caused a smaller reversible inhibition of EFS-induced contraction than in normal tracheal spiral ring, while muscimol inhibited EFS-induced tracheal contraction to a similar extent to that observed in normal tracheae. GABA had no effect on the tracheal contractile response to acetylcholine. CONCLUSION: The results suggest that there may be a biological mechanism mediated by prejunctional GABAb receptors which attenuates cholinergic contraction of airway smooth muscle and that dysfunction of the receptors may underlie the airway obstruction in asthmatics.

Acetylcholine↗
PubMed1998

Ultrastructural examination of corneal epithelium of spontaneously obese, hyperglycemic rats.

PURPOSE: Otsuka Long-Evans Tokushima fatty (OLETF) rats spontaneously become obese and hyperglycemic with age. We investigated whether the development of hyperglycemia would alter the ultrastructure of the corneal epithelium. METHODS: Scanning and transmission electron microscopy (SEM and TEM) were used to examine the morphology of corneal epithelial cells. Fourteen OLETF rats were evaluated, and 9 Long-Evans Tokushima Otsuka (LETO) rats were used as control. Non-hyperglycemic OLETF rats served as controls. RESULTS: SEM showed exfoliative changes in the surface of the central corneal epithelium of the hyperglycemic OLETF rats. These superficial epithelial cells were irregular in shape as compared to polygonal shapes of those of LETO and non-hyperglycemic OLETF rats. The mean anterior surface area of individual superficial epithelial cells was significantly smaller in the hyperglycemic OLETF than that of the LETO or the non-hyperglycemic OLETF rats. Central protrusion(s) could be found in some of the superficial cells of all rats examined, although this phenomenon was more common in the hyperglycemic rats than in the non-hyperglycemic rats. TEM revealed that there were numerous cytoplasmic vacuoles and wide intercellular spaces in the central corneal epithelium of the hyperglycemic OLETF rats, but not in the non-hyperglycemic rats. CONCLUSIONS: The development of spontaneous hyperglycemia in OLETF rats alters the ultrastructure of the corneal epithelium. The alterations included abnormalities of the corneal epithelial surface observed by SEM and the presence of intracellular vacuoles and enlarged intercellular spaces detected by TEM.

Animals↗