The influence of a semiconductor laser on the cell cycle of K-562 cells was investigated by flow cytometry. After semiconductor laser irradiation for 15s at a power of 500mW, the percentage of cells in the G2/M phase was increased to 31.4±1.63 (mean±SEM)% as compared with 18.5±1.26% for the untreated cells (p<0.01). Irradiation for 2 min at 100, 250, or 500mW, or for 15s at 100mW, however, did not significantly affect the cell cycle. The temperature change upon irradiation of 100-500mW, with laser light for 15s or 2min was marignal, ranging from 0.2 to 1.1°C, and no morphological change in the cells was observed after the irradiation. Based on these results, we assume that semiconductor laser irradiation under restricted conditions can activate cells in terms of their cell cycle activity by its non-thermal action
The present investigation evaluated the effectiveness of taurine in attenuating the acute nephrosis in rats following intraperitoneal administration of puromycin aminonucleoside. Animals given a single injection of aminonucleoside (100mg/kg) developed nephrotic syndrome at the end of 10 days, as evidenced by heavy proteinuria, albuminuria, and increased urinary excretion of N-acetyl-β-D-glucos-aminidase when compared with the controls. Significant increases in kidney lipid peroxides, hydroxyl radicals, and hydroperoxides were also evident. Aminonucleoside significantly reduced the levels of glutathione, total thiol, ascorbic acid, and vitamin E in the kidney tissue. Significant reduction in the activities of antioxidant enzymes such as glucose-6-phosphate dehydrogenase, superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase were also observed in the nephrotic rats. Neither saline nor saline plus taurine treatment caused detectable changes in the above biochemical variables. Daily taurine administration to nephrotic rats for 10 days, however, reduced the severity of aminonucleoside-associated renal injury with significant reduction in urinary protein constituents, decreased lipid peroxides, and increased levels of antioxidants and antioxidant enzymes. Collectively, the results of this study demonstrate a protective role of taurine in ameliorating the acute nephrosis in response to puromycin aminonucleoside administration.
The experimental results obtained from rats and guinea pigs fed a semisynthetic diet low in Se indicated no obvious changes in ultrastructure and oxidative phosphorylation of mitochondrial membranes. But the animals fed cereals from Keshan disease(KD)-endemic areas appeared to have significant abnormalities in ultrastructure and energy transduction of myocardial mitochondria: electron microscopy showed swelling of mitochondria in which the cristae were arranged in disorderly fashion and the mitochondrial membranes were less clear or even absent, the activities of succinic oxidase and cytochrome c oxidase were remarkably decreased, and the oligomycin sensitivity of H+-ATPase had a tendency to decline. However, when the diet from the KD area was supplemented with Se, all the abnormalities mentioned above were reduced significantly. The Se content of mitochondria of the animals fed either the semisynthetic diet low in Se or the diet from the KD area was lower, with statistical significance, than that of animals fed the normal diet. Supplementation of Se to the diet from KD area resulted in an increase in the Se content of mitochondria to the normal level. From the fact that the semisynthetic diet with low Se has no harmful effect on the ultrastructure and function of myocardial mitochondria it can be deduced that Se deficiency alone can not induce severe heart damage in experimental animals. Presumably, other factors in addition to Se deficiency are required for the pathogenesis of KD.
The pathogenesis of the liver damage in human erythropoietic protoporphyria is poorly understood. It has been suggested that an increased lipid peroxidation could be responsible for the hepatocellular injury in this condition. A model of mouse griseofulvin-induced protoporphyria was used for measurement of lipid peroxide formation and total iron content in the liver. Male Balb C mice had free access to standard powder diet containing 1% griseofulvin for 1 week. Excessive amounts of hepatic protoporphyria were established. The lipid peroxide level (expressed in terms of malondialdehyde) in total liver homogenate was decreased more than twice compared with that of control animals. The total content of liver iron was also significantly reduced. These results suggest that most probably lipid peroxidation does not play an essential role in the liver damage in hepatic protoporphyria.
Antineoplastic effect of adriamycin entrapped in sulfatidecontaining liposomes on colon tumor cells metastasized to the liver and preventive effect of the liposome-entrapped adriamycin on liver metastasis were studied by use of an in vivo murine model for liver metastasis made by portal injection of cells of colon 26, a murine colon cancer cell line. The levels of adriamycin in the liver at 24 and 72h after intravenous administration of the drug entrapped in sulfatide-containing liposomes were 68.2±8.7 and 47.5±12.0 nmol/g liver tissue, respectively. In the case of free adriamycin, those levels were 3.1±1.0 and 2.4±1.0nmol/g tissue. These results indicate that upon entrapment of adriamycin in the liposomes, a higher level of the drug was maintained in the liver for a longer time than the free drug. Administration of 6mg/kg of adriamycin entrapped in liposomes at 7 days after the injection of colon 26 cells brought about a significant reduction in the number of colonies on the liver surface counted at 14 days after cell injection compared with the free drug (p<0.05). The pretreatment with adriamycin entrapped in liposomes resulted in the absence of colonies in 4 of 6 mice and significantly prolonged their survival time (p<0.05). These results indicate that liposomal adriamycin is effective in the treatment of liver metastasis.
Nephrotoxic effects of stevioside and steviol on p-amino-hippurate (PAH) accumulation in rat renal cortical tissue were demonstrated. Subcutaneous administration of stevioside (1.5g/kg body weight) to rats for 9h significantly (p<0.001) decreased the ability of excised renal cortex slices to accumulate PAH in vitro by 63.4%. Stevioside had no effect on lipid peroxidation in the plasma and renal cortical slices at 9h after administration. Addition of either stevioside (6.25-100μM) or steviol (1.56-100μM) to the incubation medium inhibited PAH accumulation in the rat renal cortical slices after a 30-min incubation. This inhibitory effect was dose dependent, and was at its maximum at 25μM. Steviol was more potent than stevioside in inhibiting PAH uptake by renal cortical slices. Stevioside and steviol at a concentration of 100μM had no effect on lipid peroxidation in rat renal cortical slices incubated for 30min in vitro. These results suggest that the nephrotoxic effects induced by stevioside and steviol in rats are not related to lipid peroxidation.
Effect of chronic ethanol administration daily for 40 days together with 30% protein (HP) diet on microvillus membrane (MVM) glycosylation in rat intestine was studied. Ethanol administration to rats on a normal diet enhanced the hexose and sialic acid contents of brush borders but significantly reduced (p<0.05) membrane fucose levels. Feeding of the HP diet induced a generalized increase in MVM glycosylation. Ethanol feeding of rats maintained on the HP diet differently affected membrane glycosylation. Hexosamine content was enhanced, fucose and hexose contents were reduced, and sialic acid levels were unaltered under these conditions. The binding of 125I-wheat-germ agglutinin and 125I-peanut agglutinin to MVM was compatible with the chemical analysis of sugars in the various experimental groups. Incorporation of [14C] mannose or [14C]glucosamine into MVM from different groups of rats revealed an increase in mannosylation but a decrease in glucosamine incorporation into MVM from ethanol- or HP-fed animals. Ethanol feeding along with HP diet enhanced the incorporation of labelled sugars into MVM compared with that of the HP-fed controls. Electrophoretic distribution of radiolabelled membrane glycoproteins from the different groups revealed that glycoproteins of Mr 60, 000 were highly labelled. These results suggest that ethanol ingestion along with control or HP diet markedly modifies the intestinal MVM glycosylation but that these effects vary under different dietary regimens.
This work was designed to clarify the influence of a vitamin D3 bolus on bone metabolic turnover as manifested by serum osteocalcin, calcium, and other parameters. Bone, like other tissues, in diabetics displays microangiopathy, particularly in the case of type I diabetes. Insulin-dependent diabetics (IDD) without retinopathy (Group I, n=18), with retinopathy (Group II, n=16), and healthy persons (Group III, n=16) were studied. Fasting and 2-h postprandial serum glucose, Ca2+ (total and ionized), albumin, alkaline phosphatase (ALP), osteocalcin (OC), parathormone (PTH), 25(OH)D3, 1, 25(OH)2D3, and 24-h urinary calcium were evaluated. Diabetics were injected I.M. with 600, 000 IU of vitamin D3, and were maintained on their dietary and antidiabetic regimen. There was a significant decrease in serum Ca2+ (total and ionized), urinary calcium, OC, 1, 25(OH)2D3 and serum albumin and significant increases in glucose and ALP in both diabetic groups compared with the control. Vitamin D3 injection in diabetics led to increase in plasma 25(OH)D3 and 1, 25(OH)2D3 and decrease in PTH levels together with normalization of serum Ca2+ (total and ionized) and 24-h urinary calcium, ALP, and OC. This could be due to the specific action of vitamin D3. The insignificant difference in calcium levels and its controlling hormones between complicated and uncomplicated diabetics suggests that development of angiopathy neither exaggerates osteopathy nor impairs the osteogenic effect of vitamin D3. Hepatic and renal metabolism of the latter were intact. Vitamin D3 injection could ameliorate diabetic hyperglycaemia and improve hypoalbuminaemia.