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PubMed1976

Prenatal aspects of ascorbic acid metabolism in the albino rat.

Transfer of ascorbic acid and/or its derivatives from maternal blood into the fetus was studied during the last week of gestation in the rat. Rats were injected intravenously with [1-14C]-ascorbic acid and the rate of transfer estimated by the concentration and content of label present in placentas and fetuses. At all times studied the concentration of label in the placenta was greater than in the fetus. The highest capacity of the placenta to concentrate label was found on day 15 decreasing to a low at day 19 and again increasing up to day 21. While in the fetuses, the concentration of label per gram of tissue remained remarkably constant throughout the study. The quantity of labeled compounds transferred into the fetus per gram of placental tissue increased between day 15 and day 21 of gestation.

Animals↗

PubMed2006

Traditional cooked vegetable dishes as important sources of ascorbic acid and beta-carotene in the diets of Indian urban and rural families.

BACKGROUND: Fresh vegetable produce is abundant during the winter season in Punjab. It is an important source of vitamins and minerals in the Punjabi diet, but the availability of ascorbic acid and beta-carotene from the vegetables is altered to varying degrees when they are subjected to traditional household processing methods. OBJECTIVE: To determine the importance of traditional cooked vegetable dishes as sources of ascorbic acid and beta-carotene among urban and rural families during the winter. METHODS: Information about vegetable consumption, storage, and cooking practices was collected from 60 families, 30 each from urban and rural areas of Ludhiana District, Punjab, India. Samples of the common cooked vegetable dishes were prepared in the laboratory by methods ascertained from the survey and analyzed for ascorbic acid and beta-carotene. RESULTS: The average total daily per capita consumption of vegetables by urban and rural families was 411.7 and 365.9 g, respectively. Cooked vegetable dishes provided 68.7% of the total vegetable intake for urban families and 85.0% for rural families. On average, the edible portion constituted 78.9% of the weight of the vegetables. Ten cooked vegetable dishes that were most frequently consumed by the families (mustard saag, potato-spinach, potato-fenugreek, potato-brinjal, potato-cauliflower, potato-capsicum, potato-carrots, potato-beans, potato-peas, and cabbage-peas) were selected for preparation in the laboratory and nutritional analysis. The average concentrations of ascorbic acid and beta-carotene in the cooked vegetable dishes were 46.0 mg/100 g and 794.2 microg/100 g fresh weight, respectively. The percentage losses of ascorbic acid and beta-carotene during preparation and cooking were 26.1% and 25.9%, respectively. CONCLUSIONS: For adult Indian men and women, the recommended dietary allowance of ascorbic acid is 40 mg, and that of beta-carotene is 2,400 microg. Cooked vegetable dishes provided 269.9% and 77.5% of the recommended dietary allowances of ascorbic acid and beta-carotene, respectively, indicating that these dishes are good sources of these nutrients in the diets of both urban and rural families during the winter season.

Ascorbic Acid↗

PubMed2003

Ascorbic acid supplementation of diet for reduction of deltamethrin induced stress in freshwater catfish Clarias gariepinus.

Static bioassays were made to evaluate efficiency of supplementation of ascorbic acid to remove stress of pyrethroid pesticide deltamethrin from freshwater catfish Clarias gariepinus. Clarias gariepinus exhibited several symptoms of stress when treated with deltamethrin (0.005 mg/l) for 24 h. Hepatosomatic index, liver glycogen, ascorbic acid of blood, liver, and kidney decreased while plasma glucose levels increased. Fish previously fed for 60 days with a diet supplemented by a high level of ascorbic acid (100 mg/100 g) could remove most of the stresses. Low levels of ascorbic acid supplement did not remove the stress. Dietary supplement of ascorbic acid at also appropriate level appeared to be a good way to counter toxicity of deltamethrin to the catfish.

Animal Nutritional Physiological Phenomena↗

PubMed1989

Active transport of ascorbic acid into lens epithelium of the rat.

The transport rates of radiolabeled ascorbic acid (AA) and dehydroascorbic acid, as well as 3-O-methyl-D-glucose and L-glucose from blood into aqueous humor, lens epithelium and lens 'cortex' compartments were studied in male Sprague-Dawley rats. In vivo pulse chase kinetic studies and modeling of transport from plasma and aqueous and on into idealized water compartments of lens epithelium and cortex allowed for the calculation of transport rate constants, Ki (min-1), in experiments utilizing L-glucose as a passive internal control. TLC chromatography was used to monitor intraocular labeled molecules deriving from labeled test molecules introduced via blood. Results indicate that AA enters aqueous humor at rates similar to L-glucose and likely via simple passive diffusion. In contrast, an active uptake of AA by lens epithelium was found with the calculated entry constant for ascorbate being more than 21 times faster than that of L-glucose. Concentrations in lens epithelium were found to be more than twice that of aqueous humor within only 7 min from the introduction of a [14C]AA bolus into blood. It was also found that very little AA continued on past the epithelium to the interior lens cortex compartment. Our data suggest no special uptake of AA by lens fiber cells. The non-metabolizable analog of D-glucose, 3-O-methyl-D-glucose, however, readily moves past the lens epithelium into fiber cells at much faster rates than the passive L-glucose marker and in a manner consistent with facilitated diffusion. The data suggest that even in a nocturnal species, such as a rat, which demonstrates relatively low circulating levels of ascorbic acid in plasma and aqueous humor, special mechanisms exist for moving ascorbic acid into intraocular tissues. More specifically, the lens epithelium actively takes up ascorbate for some, as yet unclear purpose while the interior fiber cells appear to have no special uptake mechanism for this molecule.

Animals↗

PubMed2004

Ascorbic acid biosynthesis in hens producing strong and weak eggshells.

1. An experiment was conducted with two strains of layers to ascertain whether the reduction in eggshell strength occurring at the end of the production cycle is the result of reduced ascorbic acid biosynthesis. 2. Hens producing strong and weak eggshells were identified within each strain and egg production, egg weight, per cent shell, shell surface density, plasma, adrenal and hepatic ascorbic acid and renal L-gulonolactone oxidase activity were measured. 3. The strains differed in ascorbic acid synthesis, as measured by L-gulonolactone oxidase activity, and tissue ascorbic acid concentration. 4. Comparison of results from birds producing eggs of similar weight but markedly different in shell strength detected neither a shell strength group x strain interaction nor an effect of shell strength group on plasma and hepatic ascorbic acid and activity of L-gulonolactone oxidase. 5. The results did not support the hypothesis that tissue ascorbate and ascorbic acid biosynthesis are reduced in old hens producing weak eggshells.

Adrenal Glands↗

PubMed1988

Simultaneous determination of ascorbic acid and dehydroascorbic acid in cultures of C3H/10T1/2 cells.

A reproducible method is described for the separation and quantification of ascorbic acid and dehydroascorbic acid by ion-pairing reverse-phase high performance liquid chromatography and detection by absorbance at 232 nm. Lowest detectable concentrations with a linear response of detection were 5 nmol for ascorbic acid and 50 nmol for dehydroascorbic acid. This method was applied to the analysis of C3H/10T1/2 cells and culture medium after influx or efflux experiments and single or multiple treatments with ascorbic acid. Subsequent measurement of the radioactivity in the eluted fractions increased the detectability of both ascorbic acid and dehydroascorbic acid to 10 to 20 pmol.

Ascorbic Acid↗

PubMed1983

Characterization of ascorbic acid transport by adrenomedullary chromaffin cells. Evidence for Na+-dependent co-transport.

Ascorbic acid transport by bovine adrenomedullary chromaffin cells in primary cultures has been characterized. Ascorbic acid uptake can be measured by either high performance liquid chromatography with electrochemical detection or radiometric techniques with L-[1-14C]ascorbic acid. The transport system is temperature- and energy-dependent and exhibits Michaelis-Menten kinetics with an apparent Km of 29 microM when the external Na+ concentration is 150 mM. Uptake of ascorbate by chromaffin cells is ouabain-sensitive and dependent on the presence of external Na+. Ascorbate transport by chromaffin cells is, thus, an active process driven by the Na+ electrochemical gradient. The kinetics of this co-transport system fits an "affinity type" model where binding of Na+ to the carrier increases the affinity to ascorbate and vice versa. Thus, the data suggest that binding of either Na+ or ascorbate induces a conformational change in the transporter, which results in a change in the association constant for the second ligand while the mobility of the carrier remains unchanged. Cellular uptake of ascorbate into adrenomedullary chromaffin cells appears to be followed by its distribution into several subcellular compartments. One subcellular compartment for concentration of ascorbate is the chromaffin vesicle where it accumulates at a relatively slow rate. The interrelationships between ascorbate transport and other aspects of ascorbate metabolism and chromaffin vesicle function and dopamine beta-hydroxylation are also considered.

Adrenal Medulla↗

PubMed2003

Functional characterisation of the active ascorbic acid transport into cerebrospinal fluid using primary cultured choroid plexus cells.

Crossing the blood-CSF barrier is an important pathway for certain nutrients to enter the CNS. Cultured choroid plexus epithelial cells are a potent model system to study active transport properties of this tissue in vitro. In the present study this in vitro model was used to analyse ascorbic acid transport across the blood-CSF barrier that is supposedly mediated by the Na(+)-dependent transporter SVCT2. The expression of SVCT2 in the cultured cells was proven by RT-PCR. Active transport across the cell monolayer resulted in ascorbic acid enrichment at the CSF mimicking side. Ascorbic acid transport and uptake were decreased to 13 and 27%, respectively, in the presence of 200 microM phloretin. Inhibition of both transepithelial substrate transport (to 7.5%) and cytoplasmatic uptake (to 20%) was observed in Na(+)-free medium indicating that a basolaterally located and Na(+)-dependent transporter mediates ascorbic acid uptake. Substituting Cl(-) by either iodide or D-gluconate increased ascorbic acid uptake by factors of 3.7 or 2.5, respectively. Similar observations were made when Na(+)-dependent myo-inositol transport was analysed. Additionally, in presence of 100 microM bumetanide, an inhibitor of Na(+)-Cl(-)-cotransport, indirectly increased ascorbic acid and myo-inositol transport rates were observed showing that ascorbic acid-Na(+)-cotransport might balance low intracellular Na(+) concentration.

Animals↗

PubMed1995

Enhanced inhibitory effects of hyperthermia combined with ascorbic acid on DNA synthesis in Ehrlich ascites tumor cells grown at a low cell density.

Effects of hyperthermia and cell densities on inhibitory activity of ascorbic acid on DNA synthesis in Ehrlich ascites tumor cells were studied. When cells at a low density of 5 x 10(3)/ml were treated with 75 microM ascorbic acid for 1 h, DNA synthesis was inhibited after treatment at 37 degrees C and the inhibition was significantly enhanced at 42 degrees C. At a cell density as high as 1 x 10(5)/ml, however, inhibition did not occur at 37 degrees C or 42 degrees C. In contrast, dehydroascorbic acid was inactive even at a low cell density under similar conditions. Inhibitory effects of ascorbic acid on DNA synthesis were also markedly enhanced by treatment at 40 degrees C. DNA synthesis was not inhibited in the absence of the drug. Furthermore, mice transplanted with cells treated with a combination of 75 microM ascorbic acid and hyperthermia at 42 degrees C, considerably prolonged their survival time in comparison with untreated cells. Addition of ascorbic acid to hyperthermia is suggested to be an advantageous treatment for cancer.

Animals↗

PubMedDate not supplied

Spectrophotometric determination of ascorbic acid in canned fruit juices, cordials, and soft drinks with iron(III) and 1,10-phenanthroline as reagents.

A simple and accurate spectrophotometric method has been developed for the determination of ascorbic acid in canned fruit juices, cordials, and soft drinks, based on the reduction of iron(III) by ascorbic acid to iron(II), which is then complexed with 1,10-phenanthroline. Background correction is necessary for most samples and can be achieved by copper(II)-catalyzed oxidation of the acid. The calibration graph was linear from 0 to 8 micrograms/mL of ascorbic acid with a slope of 0.12/ppm. The precision for the determination of ascorbic acid in a lemon drink containing 210 micrograms/mL of the acid was 0.9%. Many ingredients commonly found in fruit juices, cordials, and soft drinks do not interfere; however, tannic acid, pyrogallol, and sulfite interfere with the method. A wide range of samples was analyzed for ascorbic acid content by the proposed method. The samples included mango and lemon tea drinks and also grapefruit juices, for which no background correction is needed.

Alcoholic Beverages↗

PubMed1989

[The content of ascorbic acids in different tissues of cattle, normally developed piglets, splay-legged piglets, adult swine and dogs].

The following ascorbic acid levels were recorded from different organs of cattle, with all values quoted being related to mg/100 g fresh matter: 150 +/- 20 in pituitary gland, 170 +/- 40 in left adrenal gland, 45.5 +/- 12.5 in spleen, 38.1 +/- 7.3 in liver, 30.0 +/- 8.5 in cerebrum, 23.2 +/- 7.2 in cerebellum, 16.4 +/- 6.1 in kidney, 11.0 +/- 2.9 in heart, and 9.1 +/- 2.1 in M. longissimus dorsi. The ascorbic acid level in blood plasma of normally developed piglets was 6.5 +/- 2.7 mg/dl and was thus higher with significance (p less than 0.01) than that recorded from splayleg piglets which was 2.3 +/- 0.96 mg/dl. The levels in the M. semimembranosus and M. semitendinosus in piglets of moderate birth weight were higher, as well (p less than 0.05). The liver level in pigs for slaughter was 30.8 +/- 9.0 mg/100 g lower than that in piglets. Piglets exhibited genetically founded differences in their capability of biosynthesis of ascorbic acid. The highest ascorbic acid level in dog was recorded from the pituitary and adrenal glands, values being 135.5 +/- 7.5 mg/100 g fresh matter or 90.3 +/- 37.8 mg/100 g. Their liver level was 27.9 +/- 11.9 mg/100 g.

Animals↗

PubMed1994

Urinary ascorbic acid--HPLC determination and application as a noninvasive biomarker of hepatic response.

A high-performance liquid chromatograph (HPLC) procedure has been developed for the determination of rat urinary ascorbic acid, a major metabolite of the hepatic glucuronic acid pathway. The presence of EDTA and HCl effectively inhibited degradation of ascorbic acid during the collection of urine specimens. The reliability of the procedure was demonstrated by its high recovery (90%), specificity (characteristic absorption maximum and discrimination from isoascorbic acid), and reproducibility (2-3% coefficient of variation). The usefulness of this assay as an indicator of hepatic response was demonstrated in preliminary experiments where increases in urinary ascorbic acid excretion were detected in male rats treated with PCB 126 (3,3',4,4',5-pentachlorobiphenyl) or PCB 105 (2,3,3',4,4'-pentachlorobiphenyl). The HPLC measurement also showed that the two PCB congeners differed markedly in their potency in stimulating urinary ascorbic acid excretion. For example, 10 micrograms/kg bw/day of PCB 126 was sufficient to cause a fourfold increase in urinary ascorbic excretion while 5000 micrograms/kg bw/day of PCB 105 was required for a sevenfold increase. In response to the administration of PCB 105 or PCB 126, urinary ascorbic acid appeared to increase to the same extent as increases in hepatic ethoxyresorufin O-deethylase (EROD) and UDP-glucuronosyltransferase (UGT) activities, and to a much higher extent than changes in liver weight and hematological and serum clinical chemical parameters. The sensitivity and specificity, the ease in obtaining timed specimens, and the noninvasive nature make this assay a useful biomarker of hepatic response in dose-finding and various acute and chronic studies.

Animals↗

PubMed2003

Ascorbic acid potentiates mitomycin C-induced micronuclei and sister chromatid exchanges in human peripheral blood lymphocytes in vitro.

Vitamin C (l-ascorbic acid), an effective free radical scavenger present as ascorbate in most biological systems, is one of the most extensively studied antioxidant vitamins. Vitamin C acts as either a free radical scavenger or a pro-oxidant producing hydrogen peroxide and free radicals. The modulatory effect of L-ascorbic acid (AA) on Mitomycin C (MMC) induced chromosome damage has been evaluated in human peripheral blood lymphocytes in vitro. The effect of L-ascorbic acid, 200 microg/ml as 1- and 2-h pretreatment on the frequencies of the biomarkers micronuclei (MN), sister chromatid exchanges (SCEs), and chromosome aberrations (CA) induced by mitomycin C 0.1 and 0.2 microg/ml has been studied. AA pretreatment caused a statistically significant increase in MMC-induced MN and SCE frequencies for all treatment groups, but did not show an increase in induced chromosome aberrations compared to MMC treatment alone. Cell division delays caused by MMC was reversed in the presence of AA. Interindividual variability in MMC as well as AA plus MMC-induced MN, SCE, and CA frequencies were evident. Ascorbic acid potentiated MMC-induced chromosome damage in human lymphocytes in vitro. The potentiation observed has to be viewed in the light of metal ion catalysed autooxidation of AA in oxygenated media and the existence of an antioxidant system in vivo that inactivates oxyradicals before their interaction with DNA.

Adult↗

PubMed1978

Adrenal function and ascorbic acid concentrations in elderly women.

Tetracosactrin (Synacthen) tests were performed on 19 elderly women who had leucocyte ascorbic acid (LAA) levels of less than 15 microgram/108 WBC. 9 were then given a daily dose of 200 mg ascorbic acid orally for 2 weeks while the other 10 were left untreated. Following this, tetracosactrin tests were repeated in both groups. All initial plasm cortisol responses to tetracosactrin were within normal limits. Treatment with ascorbic acid produced no changes in these. This suggests that the low LAA levels often found in old people do not result in adrenal insufficiency.

Adrenal Glands↗

PubMed2002

Automatic potentiometric flow titration procedure for ascorbic acid determination in pharmaceutical formulations.

A flow procedure for the determination of ascorbic acid in pharmaceutical formulations exploiting potentiometric titration is described. The method is based on the reduction of IO3- by ascorbic acid and the detection was carried out employing a flow-through ion selective electrode for iodide. The flow network controlled by a microcomputer was designed to implement multicommutation for ease of operation and robustness. The titration system allowed the determination of ascorbic acid in pharmaceutical formulations with concentrations ranging from 7.5 to 15.0 mmol l(-1). No significant differences at the 95% confidence level were observed in comparison with results obtained by a manual procedure. Merit figures of results such as a relative standard deviation of 1.0% (n=6) and a reagent consumption of 21.4 mg IO3- per determination were obtained.

Ascorbic Acid↗

PubMed1988

Influence of ascorbic acid on in vivo amidation of alpha-melanocyte stimulating hormone in guinea pig pituitary.

The effect of ascorbic acid depletion on the amidation of alphamelanocyte stimulating hormone (alpha MSH) was studied in vivo in guinea pig pituitary. After four weeks, the concentration of ascorbic acid was 1.20 +/- 0.11 mumol/g tissue (mean +/- SD) in the pituitary and 0.34 +/- 0.07 mumol/g tissue in the cerebral cortex from the depleted animals versus 7.58 +/- 0.08 and 1.51 +/- 0.32 mumol/g tissue, respectively, in the control animals. In the pituitaries from the animals depleted of ascorbate (N = 4), the relative amount of alpha MSH was reduced to approximately half the values obtained in the control group (from 66.5 +/- 4.6% of total ACTH-related peptides to 31.1 +/- 12.2% (P less than 0.0025]. A concomitant increase (from 5.9 +/- 3.1% to 19.4 +/- 4.3% (P less than 0.004] in ACTH (1-14) (the glycine-extended precursor of alpha MSH) immunoreactivity and a smaller increase in ACTH (1-39) immunoreactivity was observed in the depleted guinea pigs. Gel chromatography and reversed-phase high-performance luquid chromatography showed that the alpha MSH and ACTH (1-14) immunoreactivity was of low molecular weight and partly mono- or diacetylated. Depletion of ascorbic acid had no influence on the degree of acetylation of alpha MSH and ACTH (1-14). It is concluded that depletion of ascorbic acid reduces the in vivo amidation of ACTH (1-14) in the guinea pig pituitary.

Adrenocorticotropic Hormone↗

PubMed2006

Antioxidative effect of melatonin, ascorbic acid and N-acetylcysteine on caerulein-induced pancreatitis and associated liver injury in rats.

AIM: To investigate the role of oxidative injury in pancreatitis-induced hepatic damage and the effect of antioxidant agents such as melatonin, ascorbic acid and N-acetyl cysteine on caerulein-induced pancreatitis and associated liver injury in rats. METHODS: Thirty-eight female Wistar rats were used. Acute pancreatitis (AP) was induced by two i.p. injections of caerulein at 2-h intervals (at a total dose of 100 microg/kg b.wt). The other two groups received additional melatonin (20 mg/kg b.wt) or an antioxidant mixture containing L(+)-ascorbic acid (14.3 mg/kb.wt.) and N-acetyl cysteine (181 mg/kg b.wt.) i.p. shortly before each injection of caerulein. The rats were sacrificed by decapitation 12 h after the last injection of caerulein. Pancreatic and hepatic oxidative stress markers were evaluated by changes in the amount of lipid peroxides measured as malondialdehyde (MDA) and changes in tissue antioxidant enzyme levels, catalase (CAT) and glutathione peroxidase (GPx). Histopathological examination was performed using scoring systems. RESULTS: The degree of hepatic cell degeneration, intracellular vacuolization, vascular congestion, sinusoidal dilatation and inflammatory infiltration showed a significant difference between caerulein and caerulein + melatonin (P = 0.001), and careulein and caerulein + L(+)-ascorbic acid + N-acetyl cysteine groups (P = 0.002). The degree of aciner cell degeneration, pancreatic edema, intracellular vacuolization and inflammatory infiltration showed a significant difference between caerulein and caerulein + melatonin (P = 0.004), and careulein and caerulein + L(+)-ascorbic acid + N-acetyl cysteine groups (P = 0.002). Caerulein-induced pancreatic and liver damage was accompanied with a significant increase in tissue MDA levels (P = 0.01, P = 0.003, respectively) whereas a significant decrease in CAT (P = 0.002, P = 0.003, respectively) and GPx activities (P = 0.002, P = 0.03, respectively). Melatonin and L(+)-ascorbic acid+N-acetyl cysteine administration significantly decreased MDA levels in pancreas (P=0.03, P=0.002, respectively) and liver (P = 0.007, P = 0.01, respectively). Administration of these agents increased pancreatic and hepatic CAT and GPx activities. Melatonin significantly increased pancreatic and hepatic CAT (P = 0.002, P = 0.001, respectively) and GPx activities (P = 0.002, P = 0.001). Additionally, L(+)-ascorbic acid + N-acetyl cysteine significantly increased pancreatic GPx (P = 0.002) and hepatic CAT and GPx activities (P = 0.001, P = 0.007, respectively). CONCLUSION: Oxidative injury plays an important role not only in the pathogenesis of AP but also in pancreatitis-induced hepatic damage. Antioxidant agents such as melatonin and ascorbic acid + N-acetyl cysteine, are capable of limiting pancreatic and hepatic damage produced during AP via restoring tissue antioxidant enzyme activities.

Acetylcysteine↗

PubMed1987

Modification of iron uptake and lipid peroxidation by hypoxia, ascorbic acid, and alpha-tocopherol in iron-loaded rat myocardial cell cultures.

The ability of ascorbic acid, alpha-tocopherol, and hypoxia to modify iron uptake, chelation, and toxicity as manifested by the generation of malonyldialdehyde (MDA) was studied in myocardial cell cultures obtained from newborn rats. Exposure to 20 micrograms/ml iron provided as 59Fe-ferric ammonium citrate in serum-free Ham F-10 culture medium resulted in the accumulation of 39% of the iron within 24 hours and a 10- to 12-fold increase in cellular MDA. Hypoxia (1% oxygen) resulted in a more than twofold increase in iron uptake but only minor changes in cellular MDA concentrations. Ascorbic acid and alpha-tocopherol (1 mg/ml) had opposing effects on iron uptake and MDA production. Ascorbic acid reduced 24-hour iron uptake by 73% (P less than 0.001) whereas alpha-tocopherol increased iron uptake by 19% (P less than 0.025). In contrast, cellular MDA after iron loading increased by 86% with the addition of ascorbate, and was reduced by 75% with alpha-tocopherol (P less than 0.001). The ratio of increase in cellular MDA relative to percent iron uptake (lipid peroxidation ratio) was 7.29 with iron loading plus ascorbate vs. 0.13 with iron loading plus alpha-tocopherol, a 56-fold difference between the two extremes. In vitro deferoxamine treatment for 3 hours resulted in a 53% reduction in the radioactive iron content of iron-loaded heart cells and a 40% reduction in MDA. Simultaneous deferoxamine and ascorbate or alpha-tocopherol treatment did not affect iron mobilization, but had a profound effect on MDA concentrations. Ascorbic acid prevented entirely the beneficial effect of deferoxamine on MDA concentrations in iron-loaded cells, whereas alpha-tocopherol potentiated the effect of deferoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗