Determination of early warning signs for photocatalytic degradation of titanium white oil paints by means of surface analysis.

Titanium white (TiO2) has been widely used as a pigment in the 20th century. However, its most photocatalytic form (anatase) can cause severe degradation of the oil paint in which it is contained. UV light initiates TiO2-photocatalyzed processes in the paint film, degrading the oil binder into volatile components resulting in chalking of the paint. This will eventually lead to severe changes in the appearance of a painting. To date, limited examples of degraded works of art containing titanium white are known due to the relatively short existence of the paintings in question and the slow progress of the degradation process. However, UV light will inevitably cause degradation of paint in works of art containing photocatalytic titanium white. In this work, a method to detect early warning signs of photocatalytic degradation of unvarnished oil paint is proposed, using atomic force microscopy (AFM) and X-ray photoelectron spectroscopy (XPS). Consequently, a four-stage degradation model was developed through in-depth study of TiO2-containing paint films in various stages of degradation. The XPS surface analysis proved very valuable for detecting early warning signs of paint degradation, whereas the AFM results provide additional confirmation and are in good agreement with bulk gloss reduction.

Protein intake and lean body mass preservation during energy intake restriction in overweight older adults.

BACKGROUND: Dietary-induced weight loss is generally accompanied by a decline in skeletal muscle mass. The loss of muscle mass leads to a decline in muscle strength and impairs physical performance. A high dietary protein intake has been suggested to allow muscle mass preservation during energy intake restriction. OBJECTIVE: To investigate the impact of increasing dietary protein intake on lean body mass, strength and physical performance during 12 weeks of energy intake restriction in overweight older adults. DESIGN: Sixty-one overweight and obese men and women (63±5 years) were randomly assigned to either a high protein diet (HP; 1.7 g kg(-1) per day; n=31) or normal protein diet (NP; 0.9 g kg(-1) per day; n=30) during a 12-week 25% energy intake restriction. During this controlled dietary intervention, 90% of the diet was provided by the university. At baseline and after the intervention, body weight, lean body mass (dual-energy X-ray absorptiometry), leg strength (1-repetition maximum), physical performance (Short Physical Performance Battery, 400 m) and habitual physical activity (actigraph) were assessed. RESULTS: Body weight declined in both groups with no differences between the HP and NP groups (-8.9±2.9 versus -9.1±3.4 kg, respectively; P=0.584). Lean body mass declined by 1.8±2.2 and 2.1±1.4 kg, respectively, with no significant differences between groups (P=0.213). Leg strength had decreased during the intervention by 8.8±14.0 and 8.9±12.8 kg, with no differences between groups (P=0.689). Physical performance as measured by 400 m walking speed improved in both groups, with no differences between groups (P=0.219). CONCLUSIONS: Increasing protein intake above habitual intake levels (0.9 g kg(-1) per day) does not preserve lean body mass, strength or physical performance during prolonged energy intake restriction in overweight older adults.

Satiety and energy intake after single and repeated exposure to gel-forming dietary fiber: post-ingestive effects.

BACKGROUND: Viscous or gel-forming dietary fibers can increase satiety by a more firm texture and increased eating time. Effects of viscous or gel-forming fibers on satiety by post-ingestive mechanisms such as gastric emptying, hormonal signals, nutrient absorption or fermentation are unclear. Moreover, it is unclear whether the effects persist after repeated exposure. OBJECTIVE: To investigate satiety and energy intake after single and repeated exposure to gelled fiber by post-ingestive mechanisms. DESIGN: In a two-arm crossover design, 32 subjects (24 female subjects, 21±2 y, BMI 21.8±1.9 kg m(-2)) consumed test foods once daily for 15 consecutive days, with 2 weeks of washout. Test foods were isocaloric (0.5 MJ, 200 g) with either 10 g gel-forming pectin or 3 g gelatin and 2 g starch, matched for texture and eating time. Hourly satiety ratings, ad libitum energy intake and body weight were measured on days 1 (single exposure) and 15 (repeated exposure). In addition, hourly breath hydrogen, fasting glucose, insulin, leptin and short-chain fatty acids were measured. RESULTS: Subjects rated hunger, desire to eat and prospective intake about 2% lower (P<0.015) and fullness higher (+1.4%; P=0.041) when they received pectin compared with control. This difference was similar after single and repeated exposure (P>0.64). After receiving pectin, energy intake was lower (-5.6%, P=0.012) and breath hydrogen was elevated (+12.6%, P=0.008) after single exposure, but not after repeated exposure. Fasting glucose concentrations were higher both after single and repeated exposure to pectin (+2.1%, P=0.019). Body weight and concentrations of insulin, leptin and short-chain fatty acids did not change during the study. CONCLUSIONS: Gelled pectin can increase satiety and reduce energy intake by post-ingestive mechanisms. Although the effects were small, the effects on satiety were consistent over time, whereas the effects on energy intake reduction were not.

Transfer of chemicals from feed to animal products: The use of transfer factors in risk assessment.

The human risk assessment of feed contaminants has often been hampered by a lack of knowledge concerning their behaviour when consumed by livestock. To gain a better understanding of the transfer of contaminants from animal feed to animal products, a meta-analysis of public literature was made. Data concerning feed contaminant concentrations, feeding periods, residue levels in animal products, and other parameters were gathered and recorded. For each case a 'transfer factor', which was defined as the ratio of the concentration of a chemical in an animal product to the concentration of the chemical in animal feed, was calculated. Scientifically founded transfer factors were calculated and analysed for groups of chemicals based on their contaminant classes or physicochemical properties. These database-derived transfer factors enable a more accurate risk assessment in the case of a feed contamination, and enable rapid risk management decision-making and/or intervention.

Identification of an original non-terpenoid varnish from the early 20th century oil painting "the white horse" (1929), by h. Menzel.

Different mass spectrometric approaches were used to identify an original non-terpenoid varnish. Direct temperature-resolved MS and pyrolysis-GC/MS mainly showed the phenolic components, whereas thermally assisted (trans)methylation with tetramethylammonium hydroxide (TMAH) strongly enhanced the evidence for tung oil as part of the varnish. Transethylation studies of the fatty acids confirmed the TMAH data. The degree of hydrolysis of the oil network was found to be low. No evidence was found for a direct link between the drying oil and phenolic resin. On the basis of the MS information, the aged varnish is identified as an open-structure tert-butylphenol-formaldehyde resin which entangles the tung oil polymer.

Changes in regional brain GFAP levels and behavioral functioning following subchronic lead acetate exposure in adult rats.

Adult male WAG/Rij/MBL rats were dosed with lead acetate at 0, 4.0, 8.0 or 12.5 mg/kg, 5 days per week for 4 weeks. Animals were assessed prior to exposure, at the end of the 4-week exposure period and after a 2-week recovery period using a functional observational battery (FOB) and motor activity assessment. Rats were sacrificed two weeks after the last test session and glial fibrillary acidic protein (GFAP) concentrations were measured in eight selected brain regions. A dose-dependent decrease in motor activity was observed immediately following the end of the exposure period with no differences observed 2 weeks after cessation of exposure. Alterations in gait, decreased fore- and hindlimb grip strength, and decreased arousal were also found. Behavioral changes were accompanied by reduced weight gain and decreased body temperature during the course of exposure. GFAP concentrations were elevated in the frontal cortex, occipital cortex, striatum' and hippocampus but not in thalamus, cerebellum or brain stem. These results indicate that lead causes functional effects in the adult rat which can be detected by neurobehavioral methods. Furthermore, region-specific alterations in brain GFAP concentrations provided evidence of specificity of lead neurotoxicity in the adult brain.

Persistent alterations in regional brain glial fibrillary acidic protein and synaptophysin levels following pre- and postnatal polychlorinated biphenyl exposure.

Pregnant Wistar WU rats were exposed to 0, 5, and 25 mg of the commercial polychlorinated biphenyl (PCB) mixture Aroclor 1254 per kilogram of body weight on Days 10 to 16 of gestation. Pregnant rats were sacrificed on Gestation Day 20 to observe effects on fetal body and brain weights. Male and female offspring were sacrificed on Postnatal Days 21 and 90 (PND21 and PND90, respectively) and examined for treatment-related effects on neurochemical parameters. The concentrations of the neuronal and glial cell markers, synaptophysin and glial fibrillary acidic protein (GFAP), were measured in diverse brain regions from the offspring using immunochemical techniques. The level of calcineurin (a calmodulin-regulated protein phosphatase) activity was measured in cerebellar homogenates. In addition, ethoxyresorufin O-deethylase (EROD) activity was determined in hepatic microsomes as a measure of a well-characterized response to PCB exposure in experimental animals. The major alterations of GFAP levels following maternal PCB treatment were significant increases in the lateral olfactory tract (LOT) and the cerebellum (CB) and significant decreases in the brain stem (BS) of the offspring on PND21 and 90. Synaptophysin levels were significantly decreased relative to controls in the LOT, prefrontal cortex, and striatum of the offspring on PND90. In the BS, synaptophysin levels were significantly decreased relative to controls in male and female weanlings on PND21 and males on PND90; however, significant increases were observed in the BS of females on PND90. No effect of maternal PCB treatment was observed on levels of GFAP and synaptophysin in the dorsal hippocampus on PND21 and 90. Due to analytical restrictions statistical comparisons of GFAP levels were limited to examining the effect of maternal PCB treatment per brain region per sex per time point. Calcineurin activity was decreased in the female CB on PND21, but a significant increase in activity was observed in the female CB on PND90. No effect of maternal PCB treatment was observed on the cerebellar calcineurin activity in male offspring on PND21 and 90. EROD activity was highly induced in maternal microsomes from both PCB treatment groups, but only slightly induced in fetal hepatic microsomes. On PND21 weanling hepatic microsomal EROD activity was highly induced following gestational and lactational PCB exposure; however, on PND90 EROD activity was unaffected by maternal PCB treatment in male offspring and significantly decreased in female offspring. The results of the present study indicate that gestational and lactational exposure to the commercial PCB mixture results in long-term alterations in a neuronal and glial cell markers in specific brain regions of rats. These marker proteins may be useful for determining the structure-activity relationships in PCB-induced developmental neurotoxicity.

Regional and temporal profiles of calcium accumulation and glial fibrillary acidic protein levels in rat brain after systemic injection of kainic acid.

Cerebral calcium accumulation and increases in the astroglial intermediate filament protein, glial fibrillary acidic protein (GFAP), have been used as markers of neurotoxic and ischemic brain damage. The present study was aimed at quantitatively investigating the regional and temporal relationship of those indices following a neurotoxic insult. For this purpose, regional changes in 45Ca uptake and GFAP levels, using ELISA, were evaluated in rat brains at both early (several hours) and late time points (up to 6 months) after a single systemic injection of kainic acid (12 mg/kg). After 4 h, limbic brain areas were already heavily labelled by 45Ca. In most investigated brain areas 45Ca accumulation peaked at day 4 (maximum 5 fold increase in amygdala) and returned to normal levels within 1 week (cerebellum, pons/medulla, occipital cortex), 2 weeks (striatum, frontal cortex), 2 or 4 months (limbic brain areas), or remained significantly elevated until 6 months (thalamus). In contrast, in all investigated brain areas, except cerebellum and pons/medulla, GFAP was increased from day 2, reaching maximum levels at day 28 in most limbic structures and remained significantly elevated at the same high level (15 fold increase) in amygdala, or somewhat lower levels in other affected regions (2-7 fold), but not in the thalamus. In all brain areas with 45Ca accumulation, GFAP was increased and the peak responses were highly correlated. Thus, both indices are useful quantitative biochemical markers of acute or subchronic neurotoxicity.

Reduction of thyroxine uptake into cerebrospinal fluid and rat brain by hexachlorobenzene and pentachlorophenol.

In the present study the effects of hexachlorobenzene (HCB) and the metabolite pentachlorophenol (PCP) were investigated with respect to uptake of thyroxine (T4) into cerebrospinal fluid (CSF) and brain structures of rats. [125I]T4 was taken up into CSF of control rats by a relatively slow process, reaching a steady state after about 3 h. Both repeated dosing of HCB and single doses of PCP caused decreased uptake of [125I]T4 into CSF, total brain tissue as well as specific brain structures, such as occipital cortex, thalamus, and hippocampus. Although HCB-treatment caused a build-up of HCB and PCP levels in serum in brain only HCB was present in significant amounts (16% of the serum level). In CSF, both HCB and PCP concentrations were below detection levels. Separate experiments with PCP showed, however, a dose- and time-dependent uptake of PCP into CSF. The present results indicate that PCP and the parent compound HCB are able to affect brain supply of T4. This may have consequences for an adequate development of the brain or proper brain function in adults. The exact mechanisms of interference of PCP and/or HCB in brain uptake of T4 remain to be established.

Insertion reactions of metal carbonyl anions with methyl formate in the gas phase as revealed by (13)C- and D-labeling.

School of Chemistry, University of New South Wales, Kensington, Australia Institute of Mass Spectrometry, University of Amsterdam, Nieuwe Achtergracht The gas-phase reactions of coordinatively unsaturated metal carbonyl anions (M(CO) n (-) , M=Cr, Mn, Fe, Co; n=0-3 and Co(CO)nNO(-), n=0-2) with unlabeled and D- and (13)C-labeled methyl formate have been studied with Fourier transform ion cyclotron resonance mass spectrometry. The reactions proceed in most instances by loss of one or more CO molecules from the collision complex. In the reactions of the dicarbonyl and tricarbonyl anions with H(13)COOCH3, part of the eliminated carbon monoxide molecules contain the label revealing the occurrence of initial insertion of the metal center into the bonds adjacent to the carbonyl function of the substrate with formation of five- or six-coordinate intermediates, respectively. In addition, the MnCCO) 3 (-) , Fe(CO) 2 (-) , and CoCCO) 2 (-) ions react by the loss of methanol and a [C,H2,O] neutral species. The D- and (13)C-labeling show that methanol is expelled in a reductive elimination from a five- or six-coordinate species, whereas the [C,H2,O] loss is a more complex process possibly involving the competing losses of formaldehyde and CO + H2. In the reaction of Fe(CO) 3 (-) with H 13 (13) COOCH3, a facile consecutive exchange of all three CO ligands of the reactant ion for (13)CO is observed. This novel reaction appears to involve initial insertion into the H(13)CO-OCH3-bond followed by facile hydrogen shifts from the formyl ligand to a CO Hgand prior to the loss of unlabeled methyl formate.

Glucuronidation of thyroid hormone in rat liver: effects of in vivo treatment with microsomal enzyme inducers and in vitro assay conditions.

We investigated the effects of in vivo treatment with different microsomal enzyme inducers, including clofibrate (CLOF), hexachlorobenzene (HCB), 3-methylcholanthrene (MC), 3,3',4,4'-tetrachlorobiphenyl (TCB), and 2,3,7,8-tetrachloro-p-dioxin, as well as of in vitro addition of the detergent Brij 56 on the glucuronidation of T4, T3, and rT3 by UDP-glucuronyltransferase (UGT) activities of rat liver microsomes. The results were compared with measurements of UGT activities for bilirubin, p-nitrophenol (PNP), and androsterone. In general, glucuronidation rates were 5-fold or more higher with rT3 than with T4 or T3 as substrate. In liver microsomes from untreated rats, T4 UGT activity was stimulated by Brij 56 to a maximum of about 2-fold at 0.025% detergent. Treatment of Wistar rats for 4 days with CLOF (200 mg/kg BW.day) resulted in significant increases in UGT activities for T4 (to 154%), rT3 (to 155%), and bilirubin (to 194%), in particular if assayed in the presence of 0.025% Brij 56, but had little effect on the UGT activities for T3, PNP, and androsterone. The CLOF-induced increases in T4 and rT3 UGT activities were not observed in Gunn rats, which have a complete lack of bilirubin UGT activity and greatly impaired PNP UGT activity. Treatment of Wistar rats with a single injection of MC (50 mg/kg BW), TCB (50 mg/kg BW), or 2,3,7,8-tetrachloro-p-dioxin (6.25 micrograms/kg BW) resulted, after 4 days, in 6.3- to 7.3-fold increases in T4 UGT activity and 15.1- to 16.7-fold increases in rT3 UGT activity if determined in the absence of Brij 56, whereas T4 UGT activity was only increased by 33-68% when assayed in the presence of Brij 56. T3 glucuronidation was not affected (with Brij 56) or was increased by only 33-68% (without Brij 56) after treatment with these MC-type inducers. PNP UGT activity was induced 3.6- to 4.3-fold, whereas bilirubin and androsterone UGT activities were changed little by these treatments. Similar findings regarding T4, rT3, PNP, and bilirubin UGT activities were obtained after chronic treatment of WAG rats with HCB, another MC-type inducer. However, WAG rats lack androsterone UGT and show low T3 UGT activity, which was increased about 2.3-fold by HCB treatment. On the basis of these and previous findings it is concluded that at least three UGT isoenzymes are involved in the glucuronidation of thyroid hormone.(ABSTRACT TRUNCATED AT 400 WORDS)

Hexachlorobenzene-induced hypothyroidism. Involvement of different mechanisms by parent compound and metabolite.

Rats received repeated oral treatment with different doses of hexachlorobenzene (HCB) (0-3.5 mmol/kg) for 2 or 4 weeks. Measurements of thyroid hormone status after 2 weeks showed a dose-dependent decrease of total thyroxine (TT4) levels, decreased free thyroxine (FT4) levels and little change of total triiodothyronine (TT3) levels. The effects on thyroid hormone status were more pronounced after 4 weeks and also included increased thyroid stimulating hormone (TSH) levels. These conditions suggest that HCB had induced hypothyroidism in these animals. Indications for occupation of thyroid hormone binding proteins were found in serum of exposed animals. The major metabolite pentachlorophenol (PCP) also caused, by competitive interactions with thyroid hormone binding proteins in serum, a rapid and dose-dependent decrease of TT4 and FT4 levels, but not of TT3 levels in serum. The decrease of serum TT4 levels by repeated dosing with 3.5 mmol HCB/kg for 4 weeks could be attributed to competitive interactions of PCP with hormone serum binding proteins and to increased metabolism induced by HCB to an equal degree. At lower dose levels or with shorter dosing periods, increased metabolism of T4 is the main cause of decreased TT4 serum levels. This is the first indication that a similar effect is caused simultaneously by the parent compound and its metabolite through different and independent mechanisms.

Increased glucuronidation of thyroid hormone in hexachlorobenzene-treated rats.

Metabolism of thyroid hormones was investigated in WAG/MBL rats that had been exposed to hexachlorobenzene (HCB). Serum thyroxine (T4) levels were lowered by 35.5%, whereas triiodothyronine (T3) levels were not changed. Bile flow, as well as T4 excretion in bile were increased by HCB treatment. Analysis of bile by HPLC revealed a more than 3-fold increase of T4 glucuronide (T4G) and a concomitant reduction of non-conjugated T4. T4 UDP-glucuronyltransferase activity (T4 UDPGT) activity in hepatic microsomes was increased more than 4.5-fold in animals exposed to HCB. p-Nitrophenol (PNP) UDPGT showed a comparable increase by HCB. Both T3 and androsterone UDPGT activities were low in WAG/MBL rats compared with normal Wistar rats. T3 UDPGT activity was increased 2.5-fold by HCB, but androsterone UDPGT activity was unchanged. These results suggest that T4 is a substrate for HCB-inducible PNP UDPGT and T3 for androsterone UDPGT. In the absence of the latter, T3 is also glucuronidated to some extent by PNP UDPGT. Type 1 iodothyronine deiodinase activity was decreased by HCB treatment. It is concluded that decreased T4 levels in serum of animals after exposure to HCB may be due to a combined effect of displacement of T4 from carriers, an increased glucuronidation of T4 and enhanced bile flow.

Hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone: interaction with thyroxine binding sites of rat thyroid hormone carriers ex vivo and in vitro.

Previous results have indicated that hexachlorobenzene (HCB)-induced hypothyroidism may be caused by its main metabolite pentachlorophenol (PCP), and by tetrachlorohydroquinone (TCHQ), rather than by the parent compound. In the present experiments it was investigated whether hormone displacement from serum carriers could be a factor in the development of this hypothyroidism. In an in vitro competition assay PCP was an effective competitor for the thyroxine (T4)-binding sites of serum carriers, whereas HCB was ineffective. Ex vivo experimental results demonstrated occupation of T4-binding sites in sera from PCP-exposed animals but not in sera from HCB- or TCHQ-treated animals. Competing ability for T4-binding sites was still present in sera of PCP-exposed animals but was absent in HCB- or TCHQ-exposed animals. The results suggest that thyroid hormone displacement by the major metabolite PCP may play a role in HCB-induced hypothyroidism.

Effects of hexachlorobenzene and its metabolites pentachlorophenol and tetrachlorohydroquinone on serum thyroid hormone levels in rats.

Effects of administration of equimolar doses of hexachlorobenzene (HCB) and its metabolites pentachlorophenol (PCP) and tetrachlorohydroquinone (TCHQ) on serum thyroxine (TT4) and triiodothyronine (TT3) levels in rats were studied. Furthermore, it was investigated whether the observed effects were related to the serum levels of HCB or PCP. Rats received either corn oil (controls) or HCB, PCP or TCHQ in a single equimolar intraperitoneal dose of 0.056 mmol/kg. Results indicated that HCB did not alter serum TT4 and TT3 levels for a period up to 96 h after dosing. In contrast, PCP and TCHQ were both capable of reducing serum TT4 levels with a maximum effect between 6 and 24 h after exposure. TCHQ was more effective in repressing TT3 than TT4 blood levels. Dose-response experiments were carried out in order to obtain insight into the sensitivity of the observed effects. Rats received different doses of PCP or TCHQ intraperitoneally. The reductions of TT4 levels by PCP were inversely related to serum PCP levels in exposed animals, based on the toxicokinetics and dose-response profiles. Furthermore, PCP serum levels after HCB administration appeared too low to cause an effect. The results of this study indicate that not HCB itself, but rather its metabolites PCP and TCHQ may be involved in reduced serum thyroid hormone levels after HCB administration.

Interactions of halogenated industrial chemicals with transthyretin and effects on thyroid hormone levels in vivo.

Previous results in experimental systems have suggested that hydroxylated PCBs may decrease thyroid hormone levels through associative interaction with transthyretin. In the present paper it was investigated whether this property was also shared by various industrial chemicals, mainly pesticides. In total, 65 compounds from 12 chemical groups were analyzed for direct interference with the T4 binding site of transthyretin using a competitive binding assay. Sixty per cent of the compounds were competitive at a concentration level of 100 microM. Relatively strong interactions were observed by several chlorophenols, chlorophenoxy acids and nitrophenols, as well as by individual compounds such as hexachlorobenzene, dicofol, bromoxynil and tetrachlorohydroquinone. Examples from these chemical groups, e.g. pentachlorophenol, 2,4-dichlorophenoxybutyric acid, dinoseb and bromoxynil, also reduced plasma TT4 levels in rats. In addition, bromoxynil decreased plasma TT3 levels. The results suggest the existence of a number of halogenated industrial chemicals with a potential for lowering plasma thyroid hormone levels through interference with hormone transport carriers.

Interaction of chlorinated phenols with thyroxine binding sites of human transthyretin, albumin and thyroid binding globulin.

Previous results (Brouwer and van den Berg, Toxicol. Appl. Pharmacol., 85 (1986) 301) indicated preferential binding of a hydroxylated metabolite of tetrachlorobiphenyl to transthyretin (TTR) a carrier of thyroxine (T4). In the present study it was investigated whether the T4 binding site of TTR could be occupied specifically by hydroxylated chlorinated aromatic compounds using chlorinated phenol congeners as model compounds in a competition assay with [125I]T4. Chlorinated aromatics such as 2,3-dichlorobenzene and 3,4,3',4'-tetrachlorobiphenyl, and phenols such as 4-hydroxybiphenyl and phenol were inefficient competitors. All chlorinated phenols tested were competitors for the T4 binding site of TTR. The ranking in competition was pentachlorophenol (PCP) greater than trichlorophenols greater than dichlorophenols greater than monochlorophenols. Structures with chlorine in both ortho positions to the hydroxyl group were more efficient competitors. The relative affinity of binding of pentachlorophenol (PCP) to TTR was about twice that of T4. Scatchard analysis showed that PCP mainly decreased the affinity constant K11 while the binding capacity R1 was not altered, indicating a competitive type of inhibition. PCP was also able to compete with T4 sites on albumin with a relative affinity of 0.25. T4 binding to thyroid binding globulin (TBG) was much less affected by interference of PCP (relative affinity 0.001). The results indicate a specific interaction of chlorophenols with the T4 binding site of TTR.

Marked alterations in retinoid homeostasis of Sprague-Dawley rats induced by a single i.p. dose of 10 micrograms/kg of 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Interference of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in retinoid homeostasis was investigated in Sprague-Dawley rats with a low (dietary induced) retinoid status, that were fed a [3H]retinol-containing diet (37 MBq, 10,000 IU/kg diet) for 21 days to facilitate determination of retinoid concentrations in various tissues. The rats were exposed to a single i.p. dose of 10 micrograms TCDD/kg body weight in corn oil, or to corn oil at day 7 of [3H]retinol supplementation. TCDD induced significant reductions in retinol and retinyl ester concentrations and [3H] retinol-derived radioactivity in the liver, the lung, the intestine and the adrenals to 3-5%, 40-45%, 37%, and 56% of control values, respectively, at 14 days after exposure. In contrast, the retinoid concentrations and the amount of [3H]retinol-derived radioactivity in the kidney and serum of TCDD-treated rats was increased to 440% and 140% of corn oil-treated controls, respectively, at the termination time of the experiment. Analysis of the amount of serum retinol binding protein (RBP) by gel-permeation chromatography revealed an 150% increase in the free fraction of retinol-RBP, i.e., uncoupled to transthyretin (TTR), in serum of TCDD-treated rats. In addition, urinary excretion of [3H]retinol-derived radioactivity was significantly enhanced (to 140% of controls) by TCDD. These data indicate that TCDD induces an increased mobilization of retinoids from hepatic and extrahepatic storage sites into serum accompanied by an enhanced elimination via the kidney into the urine of rats.