Search

Synopsis The catalytic formation of hydroxyl radicals in oxidative hair colourant systems in the presence of added copper ions was measured and quantified using a colorimetric probe N, N′-(5-nitro-1,3-phenylene)bisglutaramide. Also monitored in the same experiments was the decomposition of hydrogen peroxide. The first set of experiments was performed using aqueous model solutions containing the key oxidant actives in a hair colourant, ammonium hydroxide and hydrogen peroxide at p H 10, with added copper and calcium ions. The second set of experiments was performed in the presence of hair containing different levels of copper in conditions very close to those found during hair colouring. Both sets of experiments demonstrate the ability of copper ions to trigger the formation of hydroxyl radicals and catalyse the decomposition of hydrogen peroxide. The ability of chelants ethylenediamine tetraacetic acid (EDTA) and N, N′-ethylenediamine disuccinic acid ( EDDS) to moderate the flux of hydroxyl radicals formed in solution systems was demonstrated in the presence of copper ions alone. However, only EDDS was successful in the presence of both calcium and copper ions. This was confirmed in the hair experiments where again only EDDS was successful at preventing hydroxyl radical formation where hair is added as the source of copper and calcium ions. These results are explained using metal speciation modelling and demonstrate the importance of the chelant to be able to specifically bind and prevent the one-electron redox chemistry of copper in the presence of high levels of calcium ions as found in hair. The formation of hydroxyl radicals during the colouring process was shown to lead to hair structure damage as measured by protein loss. EDDS was demonstrated to significantly reduce cuticle damage by suppressing the formation of the hydroxyl radicals in systems with realistic concentrations of calcium and copper. [ABSTRACT FROM AUTHOR]

Synthesis of sulphated proteoglycans by cell lines derived from explants of 7 rheumatoid and 9 normal specimens of synovial tissue, as well as by 7 lines of skin fibroblasts from non-rheumatoid patients, was examined. Cells of all 3 types were cultured as monolayers. They were then disaggregated and their capacity to synthesise proteoglycan estimated in cell suspensions by the incorporation of [35S]-sulphate into CPC-precipitable material during 2 hours of incubation. Cell suspensions incorporated somewhat more [35S]-sulphate than corresponding duplicate monolayers. Synovial cells from rheumatoid patients incorporated 2 to 3 times as much [35S]-sulphate as synovial cells from normals. Skin fibroblasts, however, incorporated less [35S]-sulphate than rheumatoid or normal synovial cells up to the fifth passage. Thereafter their incorporation gradually increased to overtake that of synovial cells. About one-half to one-third of the total [35S]-sulphate labelled material was closely associated with cells from synovial tissues and fibroblasts respectively. [ABSTRACT FROM PUBLISHER]

This work aims to determine the roles of reactive oxygen species HO∙ and HO 2 - in the bleaching of melanins by alkaline hydrogen peroxide. Experiments using melanosomes isolated from human hair indicated that the HO∙ radical generated in the outside solution does not contribute significantly to bleaching. However, studies using soluble Sepia melanin demonstrated that both HO 2 - and HO∙ will individually bleach melanin. Additionally, when both oxidants are present, bleaching is increased dramatically in both rate and extent. Careful experimental design enabled the separation of the roles and effects of these key reactive species, HO∙ and HO 2 - . Rationalisation of the results presented, and review of previous literature, allowed the postulation of a simplified general scheme whereby the strong oxidant HO∙ is able to pre-oxidise melanin units to o-quinones enabling more facile ring opening by the more nucleophilic HO 2 - . In this manner the efficiency of the roles of both species is maximised., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The objective of this work was to examine the variables that influence the interaction between water hardness metals and human hair. Hair extracts various constituents from the tap water used during daily hygiene practices and chemical treatments. Calcium and magnesium metal ions are the most prevalent and give water "hardness." Inductively coupled plasma atomic emission spectroscopy (ICP-AES) was employed to quantify the metal content of hair, which was studied as a function of the following variables: hair condition (oxidative damage), level of water hardness, and water pH. We have demonstrated that these variables impact water hardness metal uptake to varying extents, and the effects are driven primarily by the binding capacity (available anionic sites) of the hair. The condition of the hair, a key representation of the binding capacity, was most influential. Interestingly, water hardness levels had only a small effect on uptake; hair became saturated with notable amounts of water hardness metals even after repeated exposure to soft water. Water pH influenced metal uptake since side chains of hair proteins deprotonate with increasing alkalinity. These insights highlight the importance to the hair care industry of understanding the interaction between water hardness metals and hair.

During hair coloring a number of disulfide bonds in cystine are oxidized (1) to create cysteic acid, forming binding sites for metal ions such as Ca(2+ )and Cu(2+ )from tap water (2). The increased uptake of these metals can have a detrimental impact on fiber properties-for example, reducing shine and causing a poor wet and dry feel (3). In addition, the increased uptake of copper can also contribute to further fiber damage during subsequent coloring due to its ability to take part in metal-induced radical chemistry (4). It is important to know where in the fibers these metals are located in order to either effectively remove these metals or control their chemistry. Nanoscale secondary ion mass spectrometry (NanoSIMS) has been used to locate the calcium and copper within hair that has been treated with a colorant and washed multiple times in tap water containing these ions. Untreated hair is used as a baseline standard material. Images with up to 50-nm spatial resolution of the preferential locations of calcium uptake were obtained, showing a high concentration of calcium in the cuticle region of colored hair, specifically in the sulfur-rich regions (A-layer and exocuticle).

High-pressure differential scanning calorimetry (HPDSC) can be used to gain information on both the degree of crystallinity in the intermediate filaments (IFs) and the structural rigidity of the surrounding matrix or intermediate filament associated proteins (IFAP) of the hair cortex (1-3). We have used HPDSC to measure changes in the denaturation temperature (T(D)) and enthalpy (DeltaH(D)) of the crystalline components after multiple treatments with permanent hair colorant products. We have observed that after three repeat treatments both the denaturation enthalpy and peak temperature are significantly decreased vs the untreated starting substrate. However, on dialysis of the fibers in deionized water this decrease is shown to be completely reversible, returning the enthalpy and temperature to that of the untreated hair. It is proposed that the decrease is due to the incorporation of formulation components such as the alkalizer and surfactants etc. and metal ions such as calcium and magnesium from the tap wash water. These components are predicted to have a non-permanent effect on the salt bridges and hydrogen bonds and hence the rigidity or viscosity of the matrix. We have compared the denaturation temperature with the tensile properties of the fiber after treatment both before and after removal of actives from the fiber.

High Pressure Differential Scanning Calorimetry (HPDSC) can be used to gain information on both the degree of crystallinity in the intermediate filaments (IFs) and the structural rigidity of the surrounding matrix or intermediate filament associated proteins (IFAP) of the hair cortex. We have used HPDSC to measure changes in denaturation temperature (T(D)) and enthalpy (deltaH(D)) of the crystalline components after treatment with bleach products. Literature reports suggest that a decrease in peak denaturation temperature is indicative of permanent damage to the hair. However, changing the rigidity of the matrix surrounding the IFs, by temporarily changing electrostatic interactions, should also result in a similar decrease in peak temperature. The complex nature of bleach formulations including oxidants, alkalizers and salts suggests that several of the components could have a non-permanent affect on salt bridges and hydrogen bonds and hence rigidity or viscosity of the matrix. We have compared the denaturation temperature with levels of lightening (dL) and tensile properties of the fiber after treatment both before and after removal of actives from the fiber. It is evident that the HPDSC results are strongly influenced by formulation components and that these changes are reversible with extensive washing or dialysis. Combined with tensile data, it is proposed that a decrease in T(D) and deltaH(D) following treatment with bleach products can be due to both permanent and reversible changes to either the intermediate filaments or intermediate filament associated proteins of the hair fiber.

LHRH and LHRH agonists have been reported to exhibit somewhat paradoxical antireproductive effects. The current studies were undertaken to examine the actions of these substances on one parameter of ovarian function which is required for ovulation, i.e. prostaglandin production. Granulosa cells were obtained from immature rats 48 h after injection of 20 IU PMSG and incubated for up to 5 h in vitro. LHRH, [D-Ala6, des-Gly-NH2(10)]LHRH-ethylamide (Analog I) and [D-Leu6, des-Gly-NH2(10)]LHRH-ethylamide (Analog II) were observed to stimulate prostaglandin accumulation by granulosa cells. Analog I, for example, at 100 ng/ml increased PGE from 0.19 +/- 0.06 in the control to 7.7 +/- 2.01 ng/2 x 10(6) cells (n = 7; P less than 0.01) after 5 h. TRH, on the other hand, had no effect on prostaglandin accumulation. When added with LH or FSH, the stimulation by maximal concentrations of Analog I and the gonadotropins appeared additive. Although the stimulation of prostaglandin accumulation by LH appears to be mediated by cAMP, no effect of Analog I on the amount of cAMP could be detected. cAMP was determined in cells plus medium at times of 1.5 min to 5 h and at concentrations of 10-2000 ng/ml Analog I, but did not change from the control. LHRH and LHRH agonists, therefore, stimulate the accumulation of ovarian granulosa cell prostaglandins and do so in a manner apparently distinct from that of LH or FSH.

Incubation of bovine corpus luteum slices at 37 C with luteinizing hormone showed that 10.0 microng LH/ml caused a maximum rise in tissue cyclic AMP content within 15 min. Slices incubated with 1.0 or 0.1 microng LH/ml showed a much more gradual accumulation of this nucleotide. In the absence of added LH, a marked decline in the amount of cyclic AMP was observed during the first 60 min. The possible role of cyclic AMP in the action of LH was reexamined by studying the dose-response effect of LH on the stimulation of progesterone synthesis, cyclic AMP-dependent protein kinase activation, and cyclic AMP accumulation. After a 2-h incubatin, the results showed that the dose required to elicit a minimal significant stimulation of steroidogenesis was 0.01 microng/ml LH. At this and higher concentrations of LH, a concomitant stimulation of protein kinase activity and progesterone synthesis was also consistently observed. However, significant accumulation of cyclic AMP became consistently detectable only at 0.1 microng/ml LH. This report is the first to show a positive correlation between the activation of cyclic AMP-dependent protein kinase and the stimulation of steroidogenesis in the corpus luteum at the same minimal effective level of LH. These results indicate that cyclic AMP and the cyclic AMP-dependent protein kinase probably play important intermediary roles in the stimulation of steroidogenesis by LH in the bovine corpus luteum.

This investigation uses electron microscopy to examine the effect of prostaglandins on follicular tissue during the ovulatory process. The ultrastructure of follicles from indomethacin-treated rabbits was compared to the ultrastructure of normal ovulatory follicles in order to determine the morphological differences between follicles with negligible and normal prostaglandin synthesis, respectively. The most obvious difference between the two groups of follicles was that the tissue at the apex of normal follicles began to thin out significantly by 9 h post coitus (near the time of ovulation), whereas the follicles from indomethacin-treated animals showed no signs of thinning, even as late as 12 h post coitus. It appeared that the fibroblasts in the follicles with limited prostaglandin synthesis failed to undergo the normal ovulatory transformation from a quiescent to a proliferative state. Otherwise, the prostaglandin-deficient follicles had a number of morphological features similar to those which usually occur in ovulatory tissue. There was detectable loosening of the connective tissue elements and some indication of edema at the apex of the mature follicles. Also, granulocytes became localized in the vascular compartment of these follicles. In addition, there tended to be an increase in the multivesicular structures which protrude from the fibroblasts, as well as an increase in the dense granules which accumulate in the cytoplasm of the surface epithelial cells. Collectively, these data suggest that normal prostaglandin synthesis in ovulatory follicles may be important in the connective tissue decomposition and ultimate thinning of the follicle wall.

Financial and other costs of managing 194 inpatients and 433 outpatients referred to the rheumatology service of a Canadian general teaching hospital during 1978 were assessed. The tax financed institutional cost/outpatient visit was $102, compared to $112/inpatient day, which was 62% of the hospital's $180 cost/inpatient day. Hospital financial costs represent 78% of RDU outpatient costs and 85% of substantially lower than per diem rates. Our findings caution against relying solely on hospital data in assessing total economic costs of any diagnostic subset of patients.

Extracts containing uridine diphosphate (UDP) glucose dehydrogenase (EC 1.1.1.22) activity were prepared from rheumatoid and from normal human synovial cell lines using previously standardized techniques. Although no significant differences in the enzyme from the 2 sources were detected with respect to activity, substrate affinities, or responses to temperature and pH, these determinations have demonstrated that the enzyme is very sensitive to alterations in these parameters. The ultimate activity of the enzyme in vivo will be dependent upon the extent of the increased temperature, acidity, and altered glucose metabolism in the rheumatoid joint.

The subcellular localization of adenylate cyclase (ATP pyrophosphatelyase (cyclizing), EC 4.6.1.1) in bovine corpus luteum was studied using isotonic and hypotonic homogenization and fractionation conditions. All fractions prepared were assayed for adenylate cyclase, marker enzymes and DNA. Only plasma membrane marker enzyme, 5'-nucleotidase paralleled the distribution of adenylate cyclase under both isotonic and hypotonic conditions (conditionsoth isotonic and hypotonic conditions (coefficient of correlation = 0.95). Two main fractions prepared under hypotonic conditions were subfractionated by discontinuous sucrose gradient centrifugation. The highest amount of adenylate cyclase was found in a fraction having a density approximately equal to 1.13 g/cm3. The specific activity of this fraction was 4--6 times higher than that of the homogenate. The electron microscopic study of this fraction revealed the presence of a single type of particulate material consisting of small vesicles exhibiting a typical unit membrane structure. It is concluded that this adenylate cyclase is primarily localized in the plasma membranes. Basal adenylate cyclase activity of plasma membranes was stimulated 2--3 times by luteinizing hormone (10 mug/ml), 3--4 times by prostaglandin E2 (10 mug/ml), 4--6 times by NaF (0.01 M) and two times by methanol (0.2%).

In vitro conditions affecting synthesis of sulfated proteoglycans by cell suspensions derived from monolayer cell cultures of normal and rheumatoid synovial tissue were examined. The capacity of cells to synthesize proteoglycans was estimated by the incorporation of 35S--sulfate into cetylpyridinium chloride--precipitable material. Synthesis of sulfated proteoglycans was maximal during log phase, and after 2--3 hours of recovery from disaggregation. Normal synovial cells appeared to be more sensitive to changes in serum concentration than were rheumatoid synovial cells, but rheumatoid synovial cells were more sensitive to changes in cell density. The proportion of newly synthesized extracellular proteoglycans increased with the duration of incubation in 35S--sulfate.

Adenosine-3',5'-monophosphate (cyclic AMP) concentration was measured in plasma from nonpregnant women; women in the 7-41 weeks of normal pregnancy; during labor; and 5-7 h postpartum. The cyclic AMP levels in the course of normal pregnancy showed an initial peak volume at 14 weeks. After falling to nonpregnant level at 18 weeks, it began to rise steadily and reached a second peak at 34 weeks. A gradual decline was then followed until labor. The postpartum plasma concentration was significantly lower than the nonpregnant level. A similar pattern was found in serial studies in 4 women of normal pregnancy. Sequential cyclic AMP measurement in 5 hypertensive pregnancies showed a markedly elevated level during 16-26 weeks, but became comparable to normal pregnancy values thereafter. In the only preeclamptic patient studied, cyclic AMP was elevated in the 16-27th weeks although no clinical symptom was found until the 31st week. The study showed that the plasma cyclic AMP level in normal pregnancy becomes elevated above nonpregnant level at the end of the first and during the third trimesters. However, this profile appeared to be altered in pregnancies complicated by hypertension.

The purpose of this study was to determine whether estrogens exerted a direct inhibitory effect on progesterone synthesis in isolated human luteal cells in vitro. It was found that hCG stimulated progesterone synthesis by luteal cells, obtained from corpora lutea of the menstrual cycle, whereas cells isolated from corpora lutea of pregnancy were unresponsive to exogenous hCG. Estradiol markedly inhibited (P less than 0.001) this hCG effect in luteal cells of the menstrual cycle, and this inhibition was dose dependent. Estradiol did not block the stimulation of cAMP accumulated by hCG in the luteal cells of the cycle but did inhibit the stimulatory effect of dibutyryl cAMP on progesterone synthesis. These data suggest that estrogens may directly cause functional luteolysis in the human and that its site of action may be after the accumulation of cAMP.