Chromate reduction on humic acid derived from a peat soil--exploration of the activated sites on HAs for chromate removal.

Humic substances are a major component of soil organic matter that influence the behavior and fate of heavy metals such as Cr(VI), a toxic and carcinogenic element. In the study, a repetitive extraction technique was used to fractionate humic acids (HAs) from a peat soil into three fractions (denoted as F1, F2, and F3), and the relative importance of O-containing aromatic and aliphatic domains in humic substances for scavenging Cr(VI) was addressed at pH 1. Spectroscopic analyses indicated that the concentrations of aromatic C and O-containing functional groups decreased with a progressive extraction as follows: F1>F2>F3. Cr(VI) removal by HA proceeded slowly, but it was enhanced when light was applied due to the production of efficient reductants, such as superoxide radical and H(2)O(2), for Cr(VI). Higher aromatic- and O-containing F1 fraction exhibited a greater efficiency for Cr(VI) reduction (with a removal rate of ca. 2.89 mmol g(-1) HA under illumination for 3 h). (13)C NMR and FTIR spectra further demonstrated that the carboxyl groups were primarily responsible for Cr(VI) reduction. This study implied the mobility and fate of Cr(VI) would be greatly inhibited in the environments containing such organic groups.

Influence of chemical compositions and molecular weights of humic acids on Cr(VI) photo-reduction.

Humic acids (HA) strongly affect the fate of trace metals in soils and aquatic environments. One of the remarkable properties of HA is its ability to reduce Cr(VI), an extremely toxic anion. However, it is unclear which HA components are involved in Cr(VI) reduction and possess the photo-induced properties. In this study, an ultrafiltration technique was used to fractionate HAs into four fractions of different nominal molecular weights (M(w)): >100, 50-100, 10-50 and <10 kDa. Each HA fraction was characterized by spectroscopic analyses followed by examining Cr(VI) removal on each fraction of HA at pH 1-5. Spectroscopic results indicated that low-M(w) HA was enriched with polar and aromatic domains. These polar, including polar C in aliphatic region, and aromatic groups were the major sites for Cr(VI) reduction because they disappeared rapidly upon interaction with Cr(VI). As a result, low M(w) of HA exhibited greater efficiency of Cr(VI) reduction. Light induced the rapid transfer of electrons between chromate-phenol/carboxyl ester, or the formation of peroxide radicals or H(2)O(2) through the ready decay of peroxy radicals associated with polar substituents, explained the rapid scavenging of Cr(VI) on polar and aromatic groups of HAs under illumination.

Trace elements burden in geriatric hemodialysis patients: a prospective multicenter collaborative study.

INTRODUCTION: Hemodialysis therapy and the aging process have been reported to interfere with the trace element (TE) status in the body. This multicenter collaborative study on blood levels of TE in geriatric hemodialysis (HD) patients was carried out with an aim to clarify the impact of the aging process and HD therapy on the TE status in such patients. METHODS: One hundred and fifty-one HD patients (65 male, 86 female), all aged over 60 (68.2+/-3.86 y), and 112 elderly controls (58 male, 54 female) with a mean age of 67.5+/-3.03 were enrolled. All patients underwent standard HD for at least 6 months. The artificial kidneys used were hollow-fiber dialyzers of cellulose membranes. Water used for HD was prepared by reverse osmosis. Blood was collected in the morning prior to dialysis and after fasting. Atomic absorption spectrophotometry was applied to measure blood levels of Pb, Cd and Hg as well as plasma levels of Cu, Zn and Al. Data are presented as mean +/- SEM. Student's t-test and linear regression were applied for statistics. RESULTS: Our geriatric chronic HD patients showed a marked elevation of blood Al and decreased plasma Zn concentrations. The blood levels of Cu, Cd, Pb and Hg were within normal limits. The blood concentrations of Al, Cu and Pb were significantly higher in HD patients than in the normal elderly controls, whereas Cd and Hg were similar in both groups, and Zn were lower in HD patients. Plasma Zn value decreased as dialysis duration increased, however there was a reversely linear correlation between plasma Zn and age. CONCLUSIONS: This data reported can be regarded as a starting point and may serve as an insight to further studies on TE imbalances in geriatric and chronic HD populations.

Labeling of hepatic glycogen after short- and long-term stimulation of glycogen synthesis in rats injected with 3H-galactose.

The effects of short- and long-term stimulation of glycogen synthesis elicited by dexamethasone were studied by light (LM) and electron (EM) microscopic radioautography (RAG) and biochemical analysis. Adrenalectomized rats were fasted overnight and pretreated for short- (3 hr) or long-term (14 hr) periods with dexamethasone prior to intravenous injection of tracer doses of 3H-galactose. Analysis of LM-RAGs from short-term rats revealed that about equal percentages (44%) of hepatocytes became heavily or lightly labeled 1 hr after labeling. The percentage of heavily labeled cells increased slightly 6 hr after labeling, and unlabeled glycogen became apparent in some hepatocytes. The percentage of heavily labeled cells had decreased somewhat 12 hr after labeling, and more unlabeled glycogen was evident. In the long-term rats 1 hr after labeling, a higher percentage of heavily labeled cells (76%) was observed compared to short-term rats, and most glycogen was labeled. In spite of the high amount of labeling seen initially, the percentage of heavily labeled hepatocytes had decreased considerably to 55% by 12 hr after injection; and sparsely labeled and unlabeled glycogen was prevalent. The EM-RAGs of both short- and long-term rats were similar. Silver grains were associated with glycogen patches 1 hr after labeling; 12 hr after labeling, the glycogen patches had enlarged; and label, where present, was dispersed over the enlarged glycogen clumps. Analysis of DPM/mg tissue corroborated the observed decrease in label 12 hr after administration in the long-term animals. The loss of label observed 12 hr after injection in the long-term pretreated rats suggests that turnover of glycogen occurred during this interval despite the net accumulation of glycogen that was visible morphologically and evident from biochemical measurement.

Social and biological correlates of localized enamel hypoplasia of the human deciduous canine tooth.

Recent studies of teeth from prehistoric children have reported a localized, roughly circular patch of deficient enamel on the labial aspect of the primary canine, which reaches its highest prevalence in the Upper Paleolithic of Europe. This study reports social and biological correlates of 33 affected kindergarten-aged children from Vancouver, Canada (2.4% of 1,350 examined). Affected children can be characterized as coming from low-income families often of East Asian or Chinese origin in which there is a degree of milk avoidance and reduced breastfeeding. The defect appears to be due to minor physical trauma to the face approximately 6 months after birth occasioned by normal motor development, involving handling and mouthing objects, which damages the developing tooth crown through deficient cortical bone over the canine crypt. Reduced cortical bone in the face of the infant is attributed to nutritional factors, involving calcium deficiency, of the mother and/or developing infant.

Comparison of 3H-galactose and 3H-glucose as precursors of hepatic glycogen in control-fed rats.

Labeling of hepatic glycogen derived from 3H-galactose and 3H-glucose was compared shortly after intravenous injection in control-fed rats. The rats were allowed to accumulate 5-8% glycogen prior to receiving label. Fifteen minutes to 2 hours after labeling, liver was excised and processed for routine light (LM) and electron microscopic (EM) radioautography (RAG) or biochemical analysis. After injection of 3H-galactose, LM-RAGs revealed that the percentage of heavily labeled hepatocytes increased from 37% after 15 minutes to 68% after 1 hour but showed no further increase after 2 hours. alpha-Amylase treatment removed most glycogen and incorporated label; thus few silver grains were observed, indicating little incorporation of label except into glycogen. EM-RAGs demonstrated that most label occurred where glycogen was located. Biochemical analysis showed initially a high blood level of label that rapidly plateaued at a reduced level by 5 minutes. Concomitantly, glycogen labeling determined by liquid scintillation counting reflected the increases observed in the RAGs. After injection of 3H-glucose, LM-RAGs revealed that only 12% of the hepatocytes were heavily labeled at 1 hour and 20% at 2 hours. In tissue treated with alpha-amylase, glycogen was depleted and label was close to background level at each interval observed. EM-RAGs showed most grains associated with glycogen deposits. Biochemically, blood levels of label persisted at a high level for 30 minutes and tissue levels increased slowly over the 2-hour period. This study shows that incorporation from 3H-galactose was more rapid than incorporation of 3H-glucose; however, label derived from both carbohydrates appeared to be incorporated mainly into glycogen.

SERGE, the subcellular site of initial hepatic glycogen deposition in the rat: a radioautographic and cytochemical study.

Hormonal control of hepatic glycogen and blood glucose levels is one of the major homeostatic mechanisms in mammals: glycogen is synthesized when portal glucose concentration is sufficiently elevated and degraded when glucose levels are low. We have studied initial events of hepatic glycogen synthesis by injecting the synthetic glucocorticoid dexamethasone (DEX) into adrenalectomized rats fasted overnight. Hepatic glycogen levels are very low in adrenalectomized rats, and DEX causes rapid deposition of the complex carbohydrate. Investigation of the process of glycogen deposition was performed by light and electron microscopic (EM) radioautography using [3H]galactose as a glycogen precursor. Rats injected with DEX for 2-3 h and [3H]galactose one hour before being killed displayed an increasing number of intensely labeled hepatocytes. EM radioautography revealed silver grains over small (+/- 1 micron) ovoid or round areas of the cytosome that were rich in smooth endoplasmic reticulum (SER) and contained a high concentration of small dense particles. These distinct areas or foci of SER and presumptive glycogen (SERGE) were most numerous during initial periods of glycogen synthesis. After longer exposure to DEX (4-5 h) more typical deposits of cytoplasmic glycogen were evident in the SERGE regions. Several criteria indicated that the SERGE foci contained glycogen or presumptive glycogen: resemblance of the largest dense particles to beta-glycogen particles in EM; association of 3H-carbohydrate with the foci; removal of particles and label with alpha-amylase; and positive reaction with periodic acid-chromic acid-silver methenamine. The concentration of SER in the small foci and the association of newly formed glycogen particles with elements of SER suggest a role for this organelle in the initial synthesis of glycogen.

Lobular and cellular patterns of early hepatic glycogen deposition in the rat as observed by light and electron microscopic radioautography after injection of 3H-galactose.

Very low hepatic glycogen levels are achieved by overnight fasting of adrenalectomized (ADX) rats. Subsequent injection of dexamethasone (DEX), a synthetic glucocorticoid, stimulates marked increases in glycogen synthesis. Using this system and injecting 3H-galactose as a glycogen precursor 1 hr prior to sacrifice, the intralobular and intracellular patterns of labeled glycogen deposition were studied by light (LM) and electron (EM) microscopic radioautography. LM radioautography revealed that 1 hr after DEX treatment, labeling patterns for both periportal and centrilobular hepatocytes resembled those in rats with no DEX treatment: 18% of the hepatocytes were unlabeled, and 82% showed light labeling. Two hours after treatment with DEX, 14% of the hepatocytes remained unlabeled, and 78% were lightly labeled; however, 8% of the cells, located randomly throughout the lobule, were intensely labeled. An increased number of heavily labeled cells (26%) appeared 3 hr after DEX treatment; and by 5 hr 91% of the hepatocytes were intensely labeled. Label over the periportal cells at this time was aggregated, whereas centrilobular cells displayed dispersed label. EM radioautographs showed that 2 to 3 hr after DEX injection initial labeling of hepatocytes, regardless of their intralobular location, occurred over foci of smooth endoplasmic reticulum (SER) and small electron-dense particles of presumptive glycogen, and in areas of SER and distinct glycogen particles. After 5 hrs of treatment with DEX, the intracellular distribution of label reflected the glycogen patterns characteristic of periportal or centrilobular regions.