Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Neutral Red”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,441 records · Page 80Linked to original sources
PubMed1965

Mechanism of Polykaryocytosis Associated with Noncytopathic Infection by Measles Virus.

Atherton, John G. (University of Southern California, Los Angeles), Sotiros G. Chaparas, Martha Cremer, and Irving Gordon. Mechanism of polykaryocytosis associated with noncytopathic infection by measles virus. J. Bacteriol. 90:213-219. 1965.-Infection with a measles virus variant resulted not only in formation of polykaryocytes (PK) but also in formation of multicellular immunofluorescent foci (IFF) in which no cytopathic effect could be detected. The ratio of IFF to PK changed from 27 to 4 during the first passage and remained 4 after a second passage. PK were plaques. Plaque assay was linear in the presence of IFF. To investigate the mechanism of PK formation, radioautography was done on cells pulse-labeled with tritiated thymidine before virus multiplication began. The results showed that PK were formed by fusion; there were no PK whose nuclei contained no label, and the proportion of labeled nuclei (32%) and distribution of grain counts was the same in PK as in uninvolved cells, ruling out nuclear replication without concomitant cytoplasmic membrane formation as the mechanism of formation of these PK. Early in PK development, neutral red uptake was markedly increased ("red" plaques). As PK matured, hyperchromicity disappeared ("white" plaques). This sequence provided an index of rate of evolution of PK. Rate of PK maturation was more rapid at 37 than at 32 C.

Journal Article↗
PubMed1975

Induction of human cell DNA synthesis by herpes simplex virus type 2.

The effect of herpes simplex virus type 2 (HSV-2) infection on the synthesis of DNA in human embryonic fibroblast cells was determined at temperatures permissive (37 C) and nonpermissive (42 C) for virus multiplication. During incubation of HSV-2 infected cultures at 42 C for 2 to 4 days or after shift-down from 42 to 37 C, incorporation of (3H)TdR into total DNA was increased 2-to 30-fold as compared with mock-infected cultures. Analysis of the (3H)DNA suggested that host cell DNA synthesis was induced by HSV-2 infection. Induction of host cell DNA synthesis by HSV-2 also occurred in cells arrested in DNA replication by low serum concentration. The three strains of HSV-2 tested were capable of stimulating cellular DNA synthesis. Virus inactivated by UV irradiation, heat, or neutral red dye and light did not induce cellular DNA synthesis, suggesting that an active viral genome is necessary for induction.

Centrifugation, Isopycnic↗
PubMed2004

Roscovitine, a cyclin-dependent kinase inhibitor, prevents replication of varicella-zoster virus.

Understanding the interactions between varicella-zoster virus (VZV) and host cells can be addressed by using small molecule inhibitors of cellular enzymes. Roscovitine (Rosco) is a purine derivative that inhibits cyclin-dependent kinase 1 (cdk1), cdk2, cdk5, cdk7, and cdk9, which are key regulators of the cell cycle and transcription. Herpesviruses are known to interact with cell cycle proteins; thus, the antiviral effects of Rosco on VZV growth were evaluated. In a plaque reduction assay, 25 micro M Rosco prevented VZV replication, and the antiviral effect was reversible for at least up to 24 h posttreatment. Rosco also reduced expression of the major transactivator, IE62, over 48 h. Confocal microscopy studies indicated that Rosco caused the immediate-early proteins ORF4 and IE62 to abnormally localize in infected cells and prevented cell-cell spread of VZV over 48 h. Rosco was found to inhibit VZV DNA synthesis as measured by real-time PCR, and this technique was used to estimate the 50% effective concentration (EC(50)) of 14 micro M. This value was close to the EC(50) estimate of 12 micro M determined from plaque reduction assays. At 25 micro M, Rosco was not cytotoxic over 48 h in a neutral red uptake assay, and proliferation was slowed as the cells accumulated in a G(2)-like state. These results demonstrate the importance of cdk's in VZV replication and suggest that cdk inhibitors could serve as useful VZV antivirals.

Antiviral Agents↗
PubMed1975

Isolation of parietal cells from guinea-pig gastric mucosa and the immunological characterization of their antigenic structure.

A method is described for the isolation of parietal cells from the gastric mucosa of the guinea pig by enzymatic digestion with collagenase. A suspension was obtained that contained 70-80% parietal cells. About 80% of the cells were viable immediately after incubation, but viability dropped sharply after one hour. Parietal cells were identified by their morphology on light and electron microscopy, by their uptake of neutral red, by immunofluorescent staining and by carbonic anhydrase activity. Antibodies to four distinct parietal-cell antigens were obtained from rabbits immunized with the isolated parietal cells or fractions thereof. These antibodies were directed against the microsomal fraction of the parietal-cell cytoplasm, the plasma and nuclear membranes, the soluble proteins, and Castle's intrinsic factor. The antibody against the microsomal fraction, though reacting in the same way as the antibody to parietal cell canaliculi found in the serum of patients with pernicious anaemia, showed greater species specificity.

Anemia, Pernicious↗
PubMed1983

Somatostatin reduces gastric mucosal blood flow in normal subjects but not in patients with cirrhosis of the liver.

The effects of 1 and 4 micrograms/kg/h somatostatin on pentagastrin-stimulated gastric mucosal blood flow and acid secretion were investigated in 12 normal subjects and in 12 patients with cirrhosis of the liver. Each dose of somatostatin was given intravenously to six normal subjects and to six patients. Gastric mucosal blood flow was measured by the neutral red clearance of the stomach. Pentagastrin at a dose of 0.67 micrograms/kg/h stimulated acid secretion less in patients with cirrhosis of the liver than in normal subjects. In normal subjects 1 micrograms/kg/h somatostatin induced a parallel decline of gastric mucosal blood flow and gastric secretion; with 4 micrograms/kg/h somatostatin mucosal blood flow was inhibited more than gastric secretion. In patients with cirrhosis of the liver gastric mucosal blood flow remained unaffected by both doses of somatostatin, while acid secretion was slightly decreased. It is concluded that somatostatin can affect gastric mucosal blood flow independently of acid secretion. Somatostatin may be ineffective in the treatment of gastric haemorrhage in patients with cirrhosis of the liver.

Female↗
PubMed1984

Properties of oral asaccharolytic black-pigmented Bacteroides.

Bacteroides endodontalis, a newly described asaccharolytic black-pigmented Bacteroides, along with the other two recognized species of this group (B. gingivalis and B. asaccharolyticus) were studied for their susceptibility to various dyes and inhibitory agents and for some of their enzymatic activities to facilitate differentiating between them. Bacteroides endodontalis resembles B. asaccharolyticus physiologically except for the fact that the former cannot grow on media containing methylene blue, neutral red, or 3% sodium chloride, whereas B. asaccharolyticus can. On the other hand, B. endodontalis and B. gingivalis can grow on a medium containing Congo red while B. asaccharolyticus cannot.

Bacteroides↗
PubMed2002

Essential role of Ca2+ -dependent phospholipase A2 in estradiol-induced lysosome activation.

The mechanism of lysosome activation by 17beta-estradiol has been studied in mussel blood cells. Cell treatment with estradiol induced a sustained increase of cytosolic free Ca2+ that was completely prevented by preincubating the cells with the Ca2+ chelator BAPTA-AM. Estradiol treatment was also followed by destabilization of the lysosomal membranes, as detected in terms of the lysosomes' increased permeability to neutral red. The effect of estradiol on lysosomes was almost completely prevented by preincubation with the inhibitor of cytosolic Ca2+ -dependent PLA2 (cPLA2), arachidonyl trifluoromethyl ketone (AACOCF3), and was significantly reduced by preincubation with BAPTA-AM. In contrast, it was virtually unaffected by preincubation with the inhibitor of Ca2+ -independent PLA2, (E)-6-(bromomethylene)tetrahydro-3-(1-naphtalenyl)-2H-pyran-2-one (BEL). The Ca2+ ionophore A-23187 yielded similar effects on [Ca2+](i) and lysosomes. Exposure to estradiol also resulted in cPLA2 translocation from cytosol to membranes, lysosome enlargement, and increased protein degradation. These results suggest that the destabilization of lysosomal membranes following cell exposure to estradiol occurs mainly through a Ca2+ -dependent mechanism involving activation of Ca2+ -dependent PLA2. This mechanism promotes lysosome fusion and catabolic activities and may mediate short-term estradiol effects.

Actins↗
PubMed1998

Persistence of Helicobacter pylori VacA toxin and vacuolating potential in cultured gastric epithelial cells.

The vacuolating toxin A (VacA) is one of the most important virulence factors in Helicobacter pylori-induced damage to human gastric epithelium. Using human gastric epithelial cells in culture and broth culture filtrate from a VacA-producing H. pylori strain, we studied 1) the delivery of VacA to cells, 2) the localization and fate of internalized toxin, and 3) the persistence of toxin inside the cell. The investigative techniques used were neutral red dye uptake, ultrastructural immunocytochemistry, quantitative immunofluorescence, and immunoblotting. We found that VacA 1) is delivered to cells in both free and membrane-bound form (i.e., as vesicles formed by the bacterial outer membrane), 2) localizes inside the endosomal-lysosomal compartment, in both free and membrane-bound form, 3) persists within the cell for at least 72 h, without loss of vacuolating power, which, however, becomes evident only when NH4Cl is added, and 4) generally does not degrade into fragments smaller than approximately 90 kDa. Our findings suggest that, while accumulating inside the endosomal-lysosomal compartment, a large amount of VacA avoids the main lysosomal degradative processes and retains its apparent molecular integrity.

Adenocarcinoma↗
PubMed1999

An anatomic atlas of the medulla oblongata of the adult goat.

An anatomic atlas of the goat brain stem was developed for use in studies that analyze medullary neuronal groups, and factors that influence variability in the location of neuronal groups were determined. The medullas of 31 adult goats (weight, 17-88 kg) were fixed, harvested, frozen, serially sectioned, stained with 0.5% neutral red, and examined with a light microscope. Obex, the point at which the central canal opens into the fourth ventricle, was taken as the zero reference point from which the rostrocaudal and mediolateral coordinates of medullary neuronal groups were determined, whereas dorsoventral coordinates were calculated from the medullary surface. Histological variations with goat body weight were quantified, and linear regression analysis provided adjustment factors for weight in all three dimensions. Similar analysis of percentage of shrinkage on fixation and processing provided adjustment factors for precise coordinates of medullary neuronal groups. For accurate location of neuronal groups, body weight and histological procedure should be taken into account. The present study provided adjustment factors for body weight and standard histological processing to locate most major medullary neuronal groups in the adult goat.

Animals↗
PubMedDate not supplied

Cadmium nephrotoxicity assessed in isolated rat glomeruli and cultured mesangial cells: evidence for contraction of glomerular cells.

Cadmium (Cd), an important pollutant, causes severe damage at the renal tubular level. Numerous previous studies have focused upon Cd tubular nephrotoxicity. The present study of Cd-induced glomerular damage examined the vasoactive effect of Cd in freshly isolated glomeruli and mesangial cells. Glomeruli were isolated by passing rat renal cortex pulp through calibrated sieves followed by culture for outgrowth of cells. Quantitative evaluation of glomerular and cellular contractions was performed by morphometric measurement of the area with an automatized image analyzer following different incubation times with Hanks' balanced salt solution or Cd2+. Each glomerulus or mesangial cell served as its own control. Cd lethality was measured with microassay methods (neutral red, MTT uptake, and lactate dehydrogenase release), allowing the determination of an IC50. This ranged from 35 to 60 microM. CdCl2 induced a time-dependent contractile effect on isolated glomeruli; planar surface area decreases were 6.9% (1 microM), 7.5% (0.1 microM), and 7% (0.01 microM). The decrease started as soon as Cd was in contact with glomeruli and ended 40 min later: T5 (2%), T10 (3.5%), T20 (4. 2%), T30 (6.3%), T40 (7%). Cell size reduction was 19% (1 microM), 14% (0.1 microM), and 18% (0.01 microM) and was also time-dependent. To confirm that contractile events occurred during the cell shape changes, examination of the mesangial alpha-actin network was performed concurrently. These results indicate that Cd contracts glomerular structures. This may, in part, explain the reduction in glomerular filtration seen in Cd nephrotoxicity.

Actins↗
PubMedDate not supplied

The cytoprotective effects of exogenous DNA fragments.

Ultraviolet irradiation of normal human keratinocytes induces a cytotoxic effect. The chromophore for this effect is believed to be genomic DNA. However, DNA damage is known to be repaired in UVB irradiated keratinocytes. The trigger for this DNA repair is potentially damaged DNA itself. To test the hypothesis that damaged DNA can induce the host cell's own DNA repair mechanism, we treated the keratinocytes with the damaged DNA and evaluated its cytoprotective effects. We have observed that fragmented calf thymus DNA irradiated and damaged with a UVC light can induce a protective effect in cultured human keratinocytes. Keratinocytes treated with UVC damaged DNA fragments are less susceptible to UVB irradiation-induced cell death as measured by neutral red uptake. Unirradiated exogenous DNA did not induce this protective effect. Similar protective effects can be seen with irradiated salmon sperm DNA. UVC damaged DNA fragments induced 60% increase in protection in human HaCaT keratinocyte in culture to the cell death induced by UVB. Similar protection was observed with UVC irradiated oligothymidylic acid (dT3-dT5) which increased the survival of human HaCaT keratinocytes after UVB irradiated by 50%. Isolated mononucleotides, irradiated or not, do not increase UVB survivability. Cellular DNA synthesis was greatly inhibited by UVB, becoming undetectable at 40 mJ/cm(2). Exogenous treatment with damaged fragments causes immediate and significant inhibition of total cellular DNA synthesis. This inhibition was dose dependent. Cells that undergo damage to their DNA are known to inhibit endogenous DNA synthesis via p53 suppressor gene activation. This is believed to allow them sufficient time to repair the host DNA. The cellular response to exogenous damaged DNA may be a similar mechanism.

Animals↗
PubMed2001

Different effects of cyclosporine a and FK506 on potassium transport systems in MDCK cells.

BACKGROUND: Hyperkalemia and metabolic acidosis are common manifestations in patients receiving the immunosuppressive agent cyclosporine A (CsA) and the recently introduced FK506. We compared the acute toxic and antiproliferative effects as well as the effects on the transport activity of Na(+)/K(+)-ATPase and Na(+)/K(+)/2Cl(-) cotransporter of CsA and FK506 in an established cell line of distal/collecting tubule origin (MDCK cells). METHODS: MDCK cells were exposed to various concentrations of CsA or FK506 and the effects on cell viability (MTT test and neutral red uptake), plasma membrane integrity (lactate dehydrogenase (LDH) release) and cell proliferation (bromodeoxyuridine (BrdU) incorporation) were compared. For transport studies, after confluence, MDCK cells were exposed to CsA or FK506 for 48 h in the presence and absence of aldosterone. Ouabain- and bumetanide-sensitive (86)Rubidium uptake measurements were used to study the activity of the Na(+)/K(+)-ATPase and Na(+)/K(+)/2Cl(-) cotransporter at the surface of intact cells. RESULTS: After 24 h of exposure CsA reduced the number of viable cells to 50% at 30 microM, whereas for FK506 2-3 times higher concentrations had to be employed. Similarly, LDH release was stimulated tenfold by 30 microM CsA but only fourfold by 70 microM FK506. In contrast, DNA synthesis was affected at lower concentrations of FK506 than of CsA. In cells treated for 24 h BrdU incorporation was significantly inhibited by 3 microM FK506, whereas a similar inhibition required 10 microM CsA. The transport activity of Na(+)/K(+)-ATPase and of Na(+)/K(+)/2Cl(-) cotransporter were significantly decreased (37 and 63%, respectively) on CsA administration (8 microM). In CsA-treated cells the K(+) channel blockers barium (1 mM), TEA (10 mM) and quinine (1 mM) did not further inhibit the transport activities suggesting that CsA might also act via inhibition of K(+) channels. FK506 at 8 microM had no effect on Na(+)/K(+)-ATPase transport activity but stimulated Na(+)/K(+)/2Cl(-) cotransporter activity by 59%. The stimulatory effect was abolished by K(+) channel blockers indicating that recycling of K(+) might increase by FK506. The simultaneous presence of aldosterone (5 microM) protected the cells from the inhibitory effect of CsA on Na(+)/K(+)-ATPase and Na(+)/K(+)/2Cl(-) cotransporter activity. The stimulatory effect of FK506 on the Na(+)/K(+)/2Cl(-)cotransporter activity was completely abolished in the presence of aldosterone. CONCLUSIONS: Both CsA and FK506 showed acute toxicity in MDCK cells in vitro with the effects of FK506 being less pronounced. CsA and FK506 had different effects on the in vivo transport rates of the Na(+)/K(+)-ATPase and the Na(+)/K(+)/2Cl(-) cotransporter; CsA inhibited the activity of the Na(+)/K(+)-ATPase and the Na(+)/K(+)/2Cl(-) cotransporter whereas FK506 stimulated the activity of Na(+)/K(+)/2Cl(-) cotransporter. These effects were abolished by the application of aldosterone.

Aldosterone↗
PubMed2003

Local anesthetics induce human renal cell apoptosis.

Renal cell apoptosis contributes significantly to the pathogenesis of acute renal failure. Local anesthetics induce apoptosis in neuronal and lymphocytic cell lines. We examined the effects of chronic (48 h) local anesthetic treatment (lidocaine, bupivacaine and tetracaine) on human proximal tubular (HK-2) cells. Apoptosis induction was assessed by detecting poly(ADP)-ribose polymerase fragmentation, caspase activation, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining, DNA laddering and by cellular morphology. Cell death was quantified by measuring neutral red dye uptake and lactate dehydrogenase released into the cell culture medium. All 3 local anesthetics caused concentration-dependent cell death, induced HK-2 cell apoptosis and potentiated TNF-alpha induced apoptosis. Local anesthetics induced HK-2 cell apoptosis by activation of caspases 3, 6, 7, 8 and 9. ZVAD-fmk, a pan-caspase inhibitor, blocked the local anesthetic induced HK-2 cell apoptosis. Local anesthetics also inhibited the activities of anti-apoptotic kinases protein kinase B (Akt) and extracellular signal regulated mitrogen-activated protein kinase. Local anesthetic's pro-apoptotic effects are independent of sodium channel inhibition as tetrodotoxin, a selective voltage-gated sodium channel blocker, failed to mimic local anesthetic-mediated induction or potentiation of HK-2 cell apoptosis. We conclude that local anesthetics induce human renal cell apoptotic signaling by caspase activation and via inhibition of pro-survival signaling pathways.

Analysis of Variance↗
PubMedDate not supplied

Decrease in toxic potential of mixed tensides maintained below the critical micelle concentration: an in vitro study.

Sodium lauryl sulphate (SLS) is an anionic tenside widely utilized in commercial topical preparations that may cause skin irritation. It has been shown that the barrier damage caused by SLS in vivo is lower when SLS is used in combination with other tensides which are able to reduce the critical micelle concentration (CMC). The aim of our study was to evaluate if the cytotoxic effect of SLS is reduced by the association with different tensides also at concentrations well below the CMC. Normal human keratinocytes from plastic surgery were grown in serum-free medium. At subconfluency, the cells were treated with SLS at a dose of 0.0025% in combination with cocamidopropyl betaine, Tween 20 and Tween 80 at the minimum toxic dose. Following tenside treatment, the culture medium was changed, and after 24 h the cells were collected for (3)H-thymidine incorporation, the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay and neutral red (NR) uptake. The cytotoxic effect on normal human keratinocytes, as evaluated by (3)H-thymidine incorporation, MTT assay and NR uptake, was significantly decreased by the combination with all the tested tensides. The correlation between cytotoxicity and physical properties was also studied by a conductimetric assay to investigate the mechanism involved in this toxicity reduction.

Betaine↗
PubMed2004

Sympathetic innervation of the tongue in rats.

We employed a glyoxylic catecholaminergic histofluorescence method to study the sympathetic innervation present in the rat tongue. One percent neutral red was used as a counterstain. Many noradrenergic fibers were demonstrated around the blood vessels, muscles, glands and submucosa of the tongue, but not in the epithelium or papilla. In a group of rats following neurectomy, the superior cervical ganglia (SCG) were removed unilaterally or bilaterally. Changes in sympathetic innervation of the tongue were examined 14 days after SCG ganglionectomy. In those animals after unilateral SCG ganglionectomy, we found no noradrenergic histofluorescence in the ipsilateral anterior 2/3 of the tongue, although some scant fluorescence was found in the ipsilateral posterior 1/3 of the tongue. However, no noradrenergic histofluorescence could be observed in animal's bilateral SCG ganglionectomies. Our results indicate that sympathetic innervation of the tongue in rats originates in the SCG, with some cross-innervation of the sympathetic fibers occurring in the posterior 1/3 of the tongue.

Adrenergic Fibers↗
PubMedDate not supplied

Resistance of cultured human skin fibroblasts from old and young donors to oxidative stress and their glutathione peroxidase activity.

BACKGROUND: It has been suggested that oxidative stress is involved in the aging process and that the resistance of animals to oxidative stress may decrease with advancing aging. However, there are only a limited number of reports of studies on the relationship between aging and resistance to oxidative stress. OBJECTIVE: The aim of this work is to examine the relationship between the resistance of human skin fibroblasts to oxidative stress and donor age, and the relevance of antioxidant enzyme activities to this resistance. METHODS: Percent cell survival was determined by the trypan blue exclusion test and the neutral red method. Superoxide dismutase activity was assayed by the method of Oyanagi, catalase activity by the method of Aebi, and glutathione peroxidase activity by the method of Flohé and Günzler. Reduced glutathione concentration was measured by the method of Griffith. Antioxidant enzyme mRNA levels were estimated by reverse transcription polymerase chain reactions (RT-PCR). RESULTS: The percent survivals of cultured human skin fibroblasts, derived from young and old donors (referred to as young and old cells, respectively), under oxidative stress from hydrogen peroxide, linoleic acid hydroperoxide, or ultraviolet light B were examined. Old cells were more resistant to such oxidative stress than young cells. The activity of glutathione peroxidase was higher by 46.1% in old cells than in young cells, although there was no difference between their relative glutathione peroxidase mRNA levels. Further, there was no difference between their activities of copper/zinc superoxide dismutase, manganese superoxide dismutase, or catalase. However, the relative mRNA levels of copper/zinc superoxide dismutase and manganese superoxide dismutase were lower by 13.9 and 20.9% in old cells than in young cells, respectively, while there was no difference between the levels of catalase. CONCLUSIONS: These results suggest that old cells are more resistant to oxidative stress than young cells, presumably because of an increase in cellular glutathione peroxidase activity.

Adult↗
PubMed2005

Testosterone and nandrolone sensitization of brain anteroventral area of third ventricle to hypertonic NaCl-induced sympathetic response.

Androgenic steroids increase atherogenesis, thrombogenicity and endothelial dysfunction when administered in high doses, however their effects on NaCl sensitivity of the brain anteroventral area of the third ventricle (DeltaV3V) have not been explored. Sprague-Dawley male rats were anesthetized with sodium pentobarbital (40 mg/kg) and the femoral intra-arterial blood pressure and heart rate monitored through a strain-gauge blood pressure transducer and tachograph. DeltaV3V microinjections of (2 microl) 1.5 mol/l NaCl solution were done according to brain coordinates: AP = 7.0 mm, L = 1.0 mm, D = 7.5 mm through a 0.2-mm diameter stainless steel needle. The injection site was verified with 1.0 microl neutral red solution. Basal systolic blood pressure increased 37.6 and 39.6 mm Hg after testosterone (1 mg/kg/day for 20 days) and nandrolone (1 mg/kg/day for 20 days) treatment respectively; diastolic blood pressure also increased upon testosterone and nandrolone treatment in 36.4 and 53.1 mm Hg, respectively; basal heart rate did not change. Vasopressor response to 1.5 mol/l NaCl DeltaV3V microinjection was higher in testosterone-treated rats; systolic blood pressure increased 56.0 vs. 28.3 control mm Hg; diastolic blood pressure increased 54.0 vs. 25 control mm Hg. This hypertensive response was 29% longer lasting in testosterone compared to vehicle-treated rats. The same pattern of DeltaV3V sensitization to hypertonic NaCl was observed in nandrolone-treated rats. Blood lipid profile changed to a proatherogenic fashion upon testosterone and nandrolone long-term treatment; the plasma-free testosterone concentration increased from 4.9 +/- 0.9 to 36.0 +/-7.1 pg/ml with the same testosterone treatment schedule. In conclusion, long-term androgenic steroid treatment sensitizes the brain DeltaV3V region to hypertonic NaCl which in turn conducts into a sympathetic vasopressor and heart rate-stimulating action.

Androgens↗
PubMed2005

Protective effects of Ginkgo biloba leaf extracts on trichloroethylene-induced human keratinocyte cytotoxicity and apoptosis.

The objective of this study was to assess the protective effects of Ginkgo biloba leaf extracts (EGb) on trichloroethylene (TCE)-induced cytotoxicity and apoptosis in normal human epidermal keratinocytes (NHEK). Cytotoxicity was determined by neutral red uptake, and lipid peroxidation of the cells was assessed by malondialdehyde (MDA) and superoxide dismutase (SOD). Electron microscopy and flow cytometry were used to evaluate NHEK apoptosis. Treatment of NHEK with various concentrations of TCE caused a substantial decrease in cell viability. NR(50 )from the cytotoxicity assay was found to be 4.53 mM. TCE caused an increase in MDA, while an inhibition of SOD activity, in a concentration-dependent manner. Electron microscopic examination revealed typical morphologic changes of apoptosis in cells treated with TCE. Incubation of NHEK with TCE (0, 0.125, 0.5, 2.0 mM) for 4 h increased the proportion of apoptotic cells from control of 19.23% to nearly 44.35%. Pretreatment of EGb at 10-200 mg/l dose-dependently attenuated the cytotoxic effect of TCE, prevented TCE-induced elevation of lipid peroxidation and decline of antioxidant enzyme activities. Similar inhibition by EGb on TCE-mediated NHEK apoptosis was also observed. These results suggest that EGb can protect NHEK from TCE-induced cytotoxicity and apoptosis, which may be associated with the superoxide scavenging effect and enhancement of antioxidant enzyme activities.

Apoptosis↗