Enhancement of In Vivo Antioxidant Ability in the Brain of Rats Fed Tannin

The effect of the oral administration of mimosa tannin (MMT) on the rat intra-hippocampal antioxidant ability was examined. Wistar rats at the age of 6 weeks were reared for 8 weeks with the rodent diet (RD) consisting of 0.1 g/kg of MMT (RD–MMT). The antioxidant ability of rat brain was evaluated from the decay of a brain–blood-barrier permeable stable nitroxide, 3-methoxycarbonyl-2,2,5,5-tetramethylpyrrolidine-1-oxyl (PCAM) measured by the microdialysis-electron spin resonance system under a freely moving state. The decay rate of PCAM in the brain of rats fed RD–MMT was significantly larger than that of rats fed control rodent diet, which indicates the increase of the antioxidant ability in the brain of rats fed RD–MMT. In vitro study showed that MMT did not reduce PCAM directly but enhanced the reduction of PCAM by ascorbic acid. These results indicate that MMT is a potent antioxidant in vitro and in vivo.     

Investigation of in vitro and in vivo antioxidant potential of secoisolariciresinol diglucoside

The present study was designed to evaluate the in vitro and in vivo ameliorative antioxidant potential of secoisolariciresinol diglucoside (SDG). In vitro antioxidant activity of synthetic SDG was carried out using DPPH, reducing power potency, and DNA protection assays. Wistar albino rats weighing 180–220 g were used for in vivo studies and liver damage was induced in the experimental animals by a single intraperitoneal (I.P.) injection of CCl₄ (2 g/kg b.w.). Intoxicated animals were treated orally with synthetic SDG at (12.5 and 25 mg/kg b.w.) and Silymarin (25 mg/kg) for 14 consecutive days. The levels of catalase (CAT), superoxide dismutase (SOD), peroxidase (POX), and lipid peroxidase (LPO) were measured in liver and kidney homogenates. The synthetic SDG exerts high in vitro antioxidant potency as it could scavenge DPPH at a IC₅₀ value of 78.9 μg/ml and has dose-dependent reducing power potency and protected DNA at 0.5 mg/ml concentration. Oral administration of synthetic SDG at 12.5 and 25 mg/kg b.w. showed significant protection compared to Silymarin (25 mg/kg) and the activities of CAT, SOD, and POX were markedly increased (P < 0.05), whereas LPO significantly decreased (P < 0.001) in a dose-dependent manner in liver and kidney in both pre- and post-treatment groups when compared to toxin-treated group. The results of in vitro and in vivo investigations revealed that synthetic SDG at 25 mg/kg b.w. is associated with beneficial changes in hepatic enzyme activities and thereby plays a key role in the prevention of oxidative damage in immunologic system.     

In vivo and in vitro decolorization of synthetic dyes by laccase from solid state fermentation with Trametes sp. SYBC-L4

Synthetic decolorization of dyes through solid cassava residue substrate fermentation with Trametes sp. SYBC-L4 via in vivo and in vitro processes was investigated in this study. Effects of pH and mediator (1-hydroxybenzotriazole, HBT) concentration on dyes decolorization were evaluated. In vitro, decolorization ratios of dyes differed considerably in pH and increased with the increasing of HBT concentration. Crude laccase (50 U/L) derived from Trametes sp. SYBC-L4 decolorized 67.91 ± 1.25 % Congo red (100 mg/L), 94.58 ± 1.05 % aniline blue (100 mg/L) and 99.02 ± 0.54 % indigo carmine (100 mg/L) with 2.5 mM HBT at pH 4.5 in 36 h of incubation. In vivo, decolorization ratios of dyes were not enhanced by usage of the mediator. After 10 days of fermentation, decolorization ratio of Congo red (1,000 mg/kg), aniline blue (1,000 mg/kg) and indigo carmine (1,000 mg/kg) was 57.82 ± 0.84, 92.53 ± 1.12 and 97.26 ± 1.92 % without the usage of mediator at pH 4.5, respectively. Moreover, there was no obvious difference between the in vivo decolorization of aniline blue and indigo carmine in the pH range of 3.0–9.0. Results showed that Trametes sp. SYBC-L4 had great potential to be used for dyes decolorization via in vivo and in vitro processes. Moreover, in terms of pH range and mediator, in vivo decolorization with Trametes sp. SYBC-L4 was more advantageous since laccase mediator was needless and the applicable range of pH was broader.     

Health risk assessments of lithium titanate nanoparticles in rat liver cell model for its safe applications in nanopharmacology and nanomedicine

Due to their high chemical stability, lithium titanate (Li₂TiO₃) nanoparticles (LTT NPs) now are projected to be transferred into different nanotechnology areas like nano pharmacology and nano medicine. With the increased applications of LTT NPs for numerous purposes, the concerns about their potential human toxicity effects and their environmental impact are also increased. However, toxicity data for LTT NPs related to human health are very limited. Therefore we aimed to investigate toxicity potentials of various concentrations (0–1,000 ppm) of LTT NPs (<100 nm) in cultured primary rat hepatocytes. Cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. DNA damage was analyzed by scoring liver micronuclei rates and by determining 8-oxo-2-deoxyguanosine (8-OH-dG) levels. The results of MTT and LDH assays showed that higher concentrations of dispersed LTT NPs (500 and 1,000 ppm) decreased cell viability. Also, LTT NPs increased TOS (300, 500 and 1,000 ppm) levels and decreased TAC (300, 500 and 1,000 ppm) levels in cultured hepatocytes. The results of genotoxicity tests revealed that LTT NPs did not cause significant increases of micronucleated hepatocytes and 8-OH-dG as compared to control culture. In conclusion, the obtained results showed for the first time that LTT NPs had dose dependent effects on oxidative damage and cytotoxicity but not genotoxicity in cultured primary rat hepatocytes for the first time.     

Dietary daidzein,but not genistein,has a hypocholesterolemic effect in non-ovariectomized and ovariectomized female Sprague-Dawley rats on a cholesterol-free diet

We compared the effects of two major isoflavones, daidzein and genistein, on lipid metabolism in rats. Daidzein (150 mg/kg diet), genistein (150 mg/kg diet), daidzein and genistein (1:1, 300 mg/kg diet), or control diets were fed to 4 groups of 6-week-old ovariectomized (Ovx) and non-Ovx Sprague Dawley rats for 4 weeks. Dietary daidzein, but not genistein, reduced serum and hepatic total cholesterol levels significantly relative to that by the control group, regardless of whether the rats had undergone ovariectomy. Genistein did not exhibit any physiological effects on lipid levels, but did affect genes involved in cholesterol metabolism. These results indicate that daidzein and genistein may influence lipid regulation via differing modes of action.     

Tracing of Zinc Nanocrystals in the Anterior Pituitary of Zinc-Deficient Wistar Rats

The aim of this study was to trace zinc nanocrystals in the anterior pituitary of zinc-deficient Wistar rats by using autometallographic technique. Male Wistar rats (30–40 days of age, pre-pubertal period) of 40–50 g body weight were divided into the following: the ZC (zinc control) group—fed with 100 ppm zinc in diet, the ZD (zinc-deficient) group—fed with zinc-deficient (1.00 ppm) diet and the PF (pair-fed) group—received 100 ppm zinc in diet. The experiments were set for 2 and 4 weeks. Pituitary was removed and processed for the autometallographic technique. The control and pair-fed groups retained their normal morphological features. However, male Wistar rats fed on zinc-deficient diet for 2 and 4 weeks displayed a wide range of symptoms such as significant (P < 0.05) decrease in diet consumption, body weight and pituitary weight and decrease in gradation of intensity of zinc nanocrystals in the nuclei. The present findings suggest that the dietary zinc deficiency causes decreased intensity of zinc nanocrystals localization and their distribution in the pituitary thereby contributing to the dysfunction of the pituitary of the male Wistar rats. The severity of zinc deficiency symptoms progressed after the second week of the experiment. Decreased intensity of zinc nanocrystals attenuates the pituitary function which would exert its affect on other endocrine organs impairing their functions indicating that the metabolic regulation of pituitary is mediated to a certain extent by zinc and/or hypothalamus-hypophysial system which also reflects its essentiality during the period of growth.     

Chronic administration of iron and copper potentiates adipogenic effect of high fat diet in Wistar rats

The primary objective of this research project is explore a possible adipogenic effect of iron and/or copper in albino Wistar rats kept on standard (STD) and high-fat (HFD) diets. The female Wistar rats in the study were divided into eight experimental groups (n = 6). Rats maintained on STD and HFD received 3 mg/l FeSO₄·7H₂O, 4.88 mg/l CuSO₄ and a combination of 1.5 mg/l FeSO₄·7H₂O and 2.44 mg/l CuSO₄ with drinking water. Control groups were kept on STD and HFD and received pure water without metal salts. Consumption of iron and copper in the groups of rats maintained on an STD did not produce a significant increase in weight, adipose tissue content or body mass index. However, the adipocyte size and infiltration were increased in the adipose tissue of STD-fed rats receiving a mixture of iron and copper with drinking water. The rats fed iron and copper and, especially, their combination on a HFD background had a significantly higher weight gain, adipose tissue content, morphometric parameters values and adipocyte size compared to STD- and HFD-fed controls. Iron and copper consumption produced their accumulation in the rats’ adipose tissue. Moreover, the studied metals reduced adipose tissue concentration of chromium and vanadium. The lipoprotein profile and serum oxidative stress biomarkers were affected in the rats receiving the metals and STD. Hyperglycemia was observed in the rats receiving the studied metals on HFD-background. Based on the analysis of the test subjects, the study suggests that iron and copper administration, especially combined, may potentiate adipogenic effect of HFD.     

Physical Property Changes in Raw and Roasted Almonds during Gastric Digestion In vivo and In vitro

The rate of almond breakdown during gastric digestion may be influenced by structural changes that occur during roasting. The primary objective of this study was to investigate in vivo physical property changes of raw and roasted almonds during gastric digestion, using the growing pig as a model for an adult human. Seventy two male pigs were fed a meal of raw or roasted almonds and digested samples were taken 20, 60, 180, 300, 480, and 720 min after meal consumption from the proximal and distal stomach regions. Particle size distribution, rheological flow behavior, and textural attributes of gastric digesta were measured. Particle size distributions were fit to the Rosin-Rammler function to determine the median particle diameter (x₅₀) and distribution spread (b) parameters. Median particle diameter was statistically influenced by stomach region (p?<?0.0001). Evidence of gastric sieving was observed by an increased median particle diameter and narrower distribution spread in the distal region. To elucidate on textural changes of diced almonds during digestion, an in vitro study was conducted in a static gastric environment. Results indicated that a majority of textural changes occurred during the first hour of digestion, a trend unobserved in the in vivo trial. No significant differences in physical property changes were observed between raw and roasted almonds during gastric digestion in vivo as measured by particle size distribution, textural attributes, and rheological flow behavior. This suggests that raw and roasted almonds break down at a similar rate in the gastric environment.     

Effects of Fluoride and/or Sulfur Dioxide on Morphology and DNA Integrity in Rats’ Hepatic Tissue

This study was aimed to evaluate the toxic effects of fluoride (F) and/or sulfur dioxide (SO₂) on morphology and DNA integrity in liver of male rats. For this, 96 Wistar rats (12-week-old) were randomly divided into four groups after 1-week adaptive breeding: the control group, treated with deionized water; the NaF group, administered high F (100 mg NaF/L in the drinking water); the SO₂ group, with sulfur dioxide in ambient air (15 ppm SO₂, 4 h/day); and NaF + SO₂ group, treated with high F and sulfur dioxide together for 8 consecutive weeks. The body weight, liver organ coefficient, morphology, and DNA damage in the liver of rats were examined. The results showed that the body weight and liver organ coefficient were not significantly changed; however, significant pathological changes of liver tissues were observed in the NaF + SO₂ group compared with the individual treated groups and control group. Furthermore, comet assay indicated that DNA damage in liver was significantly increased in the F and/or SO₂ treatment groups at 2, 4, 6, and 8 weeks, especially at 4 weeks. These results indicate that the liver morphology and DNA integrity of rats are adversely affected by F and/or SO₂ exposure.     

Comparative In Vivo Evaluations of Curcumin and Its Analog Difluorinated Curcumin Against Cisplatin-Induced Nephrotoxicity

Curcumin, a polyphenol, has pharmacological effects including antioxidant, anti-inflammatory and anti-cancer features. In this study, we have performed comparative in vivo evaluations of CDF (curcumin difluorinated) and curcumin in cisplatin-induced nephrotoxicity in rats. Male Wistar rats were divided into four groups: (1) Control; (2) Cisplatin (7 mg/kg body wt, intraperitoneal as a single dose); (3) Cisplatin and CDF (50 mg/rat/day; for 12 days); (4) Cisplatin and curcumin (50 mg/rat/day), for 12 days). Cisplatin treated rats exhibited kidney injury manifested by increased serum N-urea and creatinine (P?<?0.001). Kidney from cisplatin treated rats also exhibited significant increase in malondialdehyde (MDA) and 8-isoprostane levels (P?<?0.001). Treatment with CDF and curcumin prevented the rise in serum N-urea, creatinine, MDA and 8-isoprostane as compared to experimental control group in kidney (P?<?0.05). Compared to curcumin, CDF had greater potential in suppressing cisplatin-induced pro-inflammatory factors NF-κB and COX-2 as well as downstream markers Nrf2 and HO-1 (P?<?0.05) in kidney. The analysis on anion transport markers (OAT1 and OAT3) showed a similar trend (CDF?>?curcumin). CDF could reduce the expression of multi-drug resistance markers OCT1, OCT2, MRP2 and MRP4 to a much greater extent than curcumin (P?<?0.05). We also demonstrate that CDF influenced the expression of p-mTOR, p-p70S6K1, p-4E-BP1 and p-Akt. These data suggest that CDF can potentially be used to reduce the chemotherapy induced nephrotoxicity thereby enhancing the therapeutic window of cisplatin. The results also proved that compared to curcumin, CDF has superior protective effect in nephrotoxicity.     

Biochemical, Histological, and Memory Impairment Effects of Chronic Copper Toxicity: A Model for Non-Wilsonian Brain Copper Toxicosis in Wistar Rat

Animal models of copper toxicosis rarely exhibit neurological impairments and increased brain copper accumulation impeding the development of novel therapeutic approaches to treat neurodegenerative diseases having high brain Cu content. The aim of this study was to investigate the effects of intraperitoneally injected copper lactate (0.15 mg Cu/100 g body weight) daily for 90 days on copper and zinc levels in the liver and hippocampus, on biochemical parameters, and on neurobehavioral functions (by Morris water maze) of male Wistar rats. Copper-administered animals exhibited significantly decreased serum acetylcholinesterase (AChE) activity and impaired neuromuscular coordination and spatial memory compared to control rats. Copper-intoxicated rats showed significant increase in liver and hippocampus copper content (99.1 and 73 % increase, respectively), 40.7 % reduction in hepatic zinc content, and interestingly, 77.1 % increase in hippocampus zinc content with concomitant increase in copper and zinc levels in serum and urine compared to control rats. Massive grade 4 copper depositions and grade 1 copper-associated protein in hepatocytes of copper-intoxicated rats were substantiated by rhodanine and orcein stains, respectively. Copper-intoxicated rats demonstrated swelling and increase in the number of astrocytes and copper deposition in the choroid plexus, with degenerated neurons showing pyknotic nuclei and dense eosinophilic cytoplasm. In conclusion, the present study shows the first evidence in vivo that chronic copper toxicity causes impaired spatial memory and neuromuscular coordination, swelling of astrocytes, decreased serum AChE activity, copper deposition in the choroid plexus, neuronal degeneration, and augmented levels of copper and zinc in the hippocampus of male Wistar rats.     

Hepatic and Hippocampus Iron Status is not Altered in Response to Increased Serum Ceruloplasmin and Serum “Free” Copper in Wistar Rat Model for Non-Wilsonian Brain Copper Toxicosis

Copper and iron dyshomeostasis has been implicated directly or indirectly in the pathogenesis of neurodegenerative diseases. Previously, we have shown the first in vivo evidence of significant increase in the hippocampus copper and zinc content with spatial memory impairments, astrocytes swelling (Alzheimer type-II cells) coupled with increase in the number of astrocytes, copper deposition in the choroid plexus, and degenerated neurons in copper-intoxicated Wistar rats. In continuation with our previous study, the aim of this study was to further investigate the effects of intraperitoneally injected copper lactate (0.15 mg Cu/100 g body weight) daily for 90 days on serum “free” copper levels, iron levels in the liver, and hippocampus by atomic absorption spectrophotometry and histopathological study of the liver and brain tissues of Wistar rats using Perls' Prussian blue (PPB) stain. A massive significant increase in serum “free” copper (79.48 % increase) along with strong correlation (r?=?0.978) was found between serum copper and serum “free” copper in copper-intoxicated rats. No significant difference was detected in hepatic and hippocampus iron levels between control and copper-intoxicated rats. PPB stain demonstrated very few scattered grade 1 haemosiderin deposits within sinusoidal cells predominantly Kupffer cells; however, brain sections were negatively stained with PPB stain. In conclusion, the current study demonstrates that chronic copper toxicity causes increase in serum “free” copper, which may serve as predisposing factor for the development of neurodegeneration and memory deficits, and grade 1 haemosiderin deposition in Kupffer cells without altering hepatic and hippocampus iron levels in male Wistar rats.     

Regional Distribution of Longevity Population and Elements in Drinking Water in Jiangjin District,Chongqing City,China

This study was carried out to determine the protective effects of lithium borate (LTB) on blood parameters and histopathological findings in experimentally induced acute cadmium (Cd) toxicity in rats. Twenty-eight male Wistar albino rats were used, weighing 200–220 g, and they were randomly divided into four groups, including one control and the following three experimental groups: a Cd group (0.025 mmol/kg), a LTB group (15 mg/kg/day orally for 5 days), and a LTB + Cd group (15 mg/kg/day orally for 5 days and Cd 0.025 mmol/kg by intraperitoneal injection on the fifth day). All the rats in the study were anesthetized with ketamine at the end of the sixth day, blood was taken from their hearts, and then the rats were decapitated. The values in the control and LTB group were usually close to each other. White blood cell (WBC), neutrophil %, and C-reactive protein (CRP) levels increased in the Cd and LTB + Cd groups while lymphocyte and monocyte levels decreased in a statistically significant manner, in comparison to the other groups. It was determined that the levels of red blood cells (RBCs), hematocrit (Htc), and hemoglobin (Hb) did not change in the groups. The levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the Cd and LTB + Cd groups significantly increased, in comparison to the other groups, while the glucose, alkaline phosphatase (ALP), albumin (ALB), and total protein (TP) levels decreased. According to histopathological findings in the control and LTB groups, the liver and kidney tissues were found to have normal histological structures. In the Cd group, severe necrotic hemorrhagic hepatitis, mild steatosis, and mononuclear cell infiltration were detected in the liver. In the LTB + Cd group, degeneration and mild mononuclear cell infiltration were found in the liver. Regarding the kidney tissue in the Cd group, severe intertubular hyperemia in both kidney cortex and medulla, as well as degeneration and necrosis in the tubulus epithelium, was observed. In the LTB + Cd group, mild interstitial hyperemia and mononuclear cell infiltration was detected. Resultantly, it can be said that LTB at this dose has non-toxic effects and some beneficial effects for liver and kidney damage caused by acute Cd toxicity.     

Effects of Different Sources and Levels of Zinc on Growth Performance,Nutrient Digestibility,and Fur Quality of Growing-Furring Male Mink (<Emphasis Type="Italic">Mustela vison</Emphasis>)

The objective of this study was to investigate the effects of different sources and levels of zinc (Zn) on growth performance, nutrient digestibility, serum biochemical parameters, and fur quality in growing-furring male mink. Animals in the control group were fed a basal diet with no Zn supplementation. Mink in the other nine treatments were fed the basal diet supplemented with Zn from either grade Zn sulfate (ZnSO₄·7H₂O), Zn glycinate (ZnGly), or Zn pectin oligosaccharides (ZnPOS) at concentrations of either 100, 300, or 900 mg Zn/kg dry matter. One hundred and fifty healthy 15-week-old male mink were randomly allocated to ten dietary treatments (n = 15/group) for a 60-day trial from mid-September to pelting in December. Mink in the Zn-POS groups had higher average daily gain than those in the control group (P < 0.05). Zn source slightly improved the feed/gain (P = 0.097). N retention was increased by Zn addition (P < 0.05). Mink supplemented with dietary Zn had higher (P < 0.05) pancreas Zn level than the control group. Fur length was greater (P < 0.05) in ZnGly and ZnPOS groups compared with the control. In addition, fur length and fur density increased (linear, P < 0.05) with Zn supplementation in the diet. In conclusion, our data show that dietary Zn addition improves growth performance by increasing nitrogen retention and fat digestibility in growing-furring mink and Z-POS is equally bioavailable to mink compared to ZnGly.     

Effect of Dietary High Molybdenum on the Cell Cycle and Apoptosis of Kidney in Broilers

The experiment was conducted with the objective of examining the effects of high molybdenum on the cell cycle and apoptosis of kidney in broilers by the methods of flow cytometry. Three hundred 1-day-old Avian broilers were randomly divided into four groups, and fed on diets as follows: control diet (Mo 13 mg/kg) and high molybdenum diets (Mo 500 mg/kg, high molybdenum group I; Mo 1,000 mg/kg, high molybdenum group II; Mo 1,500 mg/kg, high molybdenum group III) for 6 weeks. The results showed that the relative weight of kidney were higher (P?<?0.05 or P?<?0.01), and the cellular percentages of G₀/G₁ phase were lower, and cellular percentages of S phase and the proliferating index were higher in high molybdenum groups II and III than in control group (P?<?0.01). The percentage of renal cell apoptosis was increased in high molybdenum groups II and III when compared with that of control group (P?<?0.01). Immunohistochemical test showed that there were increased frequencies of positive cells containing Bax protein and decreased frequencies of positive cells containing Bcl-2 protein in high molybdenum groups II and III. It was concluded that dietary high molybdenum (1,000 mg/kg and 1,500 mg/kg) impaired the progression of renal cells from S phase to G₂M phase obviously and induced renal cell apoptosis.     

Changes in cardiac Na<Superscript>+</Superscript>/K<Superscript>+</Superscript>-ATPase expression and activity in female rats fed a high-fat diet

The aim of this study was to investigate whether the presence of endogenous estradiol alters the effects of a high-fat (HF) diet on activity/expression of the cardiac Na⁺/K⁺-ATPase, via PI3K/IRS and RhoA/ROCK signalling cascades in female rats. For this study, female Wistar rats (8 weeks old, 150–200 g) were fed a standard diet or a HF diet (balanced diet for laboratory rats enriched with 42% fat) for 10 weeks. The results show that rats fed a HF diet exhibited a decrease in phosphorylation of the α₁ subunit of Na⁺/K⁺-ATPase by 30% (p < 0.05), expression of total α₁ subunit of Na⁺/K⁺-ATPase by 31% (p < 0.05), and association of IRS1 with p85 subunit of PI3K by 42% (p < 0.05), while the levels of cardiac RhoA and ROCK2 were significantly increased by 84% (p < 0.01) and 62% (p < 0.05), respectively. Our results suggest that a HF diet alters cardiac Na⁺/K⁺-ATPase expression via molecular mechanisms involving RhoA/ROCK and IRS-1/PI3K signalling in female rats.     

Effects of Exposure to Dietary Chromium on Tissue Mineral Contents in Rats Fed Diets with Fiber

This study evaluated the effects of diets with fiber (cellulose and/or pectin) supplemented with chromium(III) on homeostasis of selected minerals in femurs, thigh muscles, livers, and kidneys of rats. For 6 weeks, male rats were fed experimental diets: a fiber-free diet (FF), a diet containing 5 % cellulose (CEL), 5 % pectin (PEC), or 2.5 % cellulose and 2.5 % pectin (CEL?+?PEC). These diets had 2.53 or 0.164 mg Cr/kg diet. The tissue levels of Ca, Mg, Zn, Fe, and Cr were determined by using atomic absorption spectrometry. Supplementing diets with Cr resulted in significantly higher Cr levels in the femurs of rats fed the CEL diet and significantly higher Cr and Fe levels in the rats fed the CEL?+?PEC diet compared to the rats fed FF diet. Muscle Ca content was significantly lower in the rats fed the CEL?+?PEC?+?Cr diet compared to the rats fed FF?+?Cr diet. The rats consuming the PEC?+?Cr diet had the highest liver Cr content. The highest kidney Zn content was observed in the rats fed diets containing Cr and one type of fiber. These results indicate that diets containing chromium at elevated dose and fiber have a significant effect on the mineral balance in rat tissues.     

Arsenic and Manganese Alter Lead Deposition in the Rat

Lead (Pb) continues to be a major toxic metal in the environment. Pb exposure frequently occurs in the presence of other metals, such as arsenic (As) and manganese (Mn). Continued exposure to low levels of these metals may lead to long-term toxic effects due to their accumulation in several organs. Despite the recognition that metals in a mixture may alter each other’s toxicity by affecting deposition, there is dearth of information on their interactions in vivo. In this work, we investigated the effect of As and Mn on Pb tissue deposition, focusing on the kidney, brain, and liver. Wistar rats were treated with eight doses of each single metal, Pb (5 mg/Kg bw), As (60 mg/L), and Mn 10 mg/Kg bw), or the same doses in a triple metal mixture. The kidney, brain, liver, blood, and urine Pb, As, and Mn concentrations were determined by graphite furnace atomic absorption spectrophotometry. The Pb kidney, brain, and liver concentrations in the metal-mixture-treated group were significantly increased compared to the Pb-alone-treated group, being more pronounced in the kidney (5.4-fold), brain (2.5-fold), and liver (1.6-fold). Urinary excretion of Pb in the metal-mixture-treated rats significantly increased compared with the Pb-treated group, although blood Pb concentrations were analogous to the Pb-treated group. Co-treatment with As, Mn, and Pb alters Pb deposition compared to Pb alone treatment, increasing Pb accumulation predominantly in the kidney and brain. Blood Pb levels, unlike urine, do not reflect the increased Pb deposition in the kidney and brain. Taken together, the results suggest that the nephro- and neurotoxicity of “real-life” Pb exposure scenarios should be considered within the context of metal mixture exposures.     

Neuroprotective Benefits of Aerobic Exercise and Organoselenium Dietary Supplementation in Hippocampus of Old Rats

The progressive decline of neurological functions, such as learning and memory, is an unavoidable consequence of aging. Our previous work suggested that the combination of physical exercise and a diet supplemented with diphenyl diselenide improves age-related memory decline in rats. The present study investigated the effects of physical exercise and a diet supplemented with diphenyl diselenide on the levels of proteins involved in the hippocampal neuroprotection to figure out the mechanisms related to the beneficial effects of this intervention in aged rats. Male Wistar rats (27 months old) were fed daily with standard chow supplemented with 1 ppm of diphenyl diselenide and subjected to swimming training with a workload (1% of body weight, 20 min/day) for 4 weeks. The hippocampus was dissected from the brain and used for the western blot and immunohistochemistry analyses. The results of this study demonstrate that the association of diphenyl diselenide-supplemented diet and swimming exercise increased the levels of proteins involved in neuroprotection and decreased the activation of those related to apoptosis and neuroinflammation in the hippocampus of old rats. This study suggests that physical exercise and a diet supplemented with (PhSe)₂ promoted neuroprotection in the hippocampus of aged rats.