Effect Of Ascorbic Acid Treatment Research Articles

Effect of ascorbic acid treatment on physicochemical and emulsifying properties of highland barley protein

The current study investigated the impact of ascorbic acid (AA) on physicochemical and emulsifying properties of highland barley protein (HBP). Emulsifying and solubility of AA-modified HBP increased compared to its native state. However, excessive AA concentration induced protein reaggregation, leading to a deterioration of these properties. At a concentration of 0.3 % (w/v) AA, the highland barley protein emulsion (HBPE) exhibited the smallest average particle size (0.59 μm), and the protein demonstrated superior emulsification properties. The observed alterations stem from the formation of covalent bonds between HBP and AA through the Maillard reaction. These changes also relate to modifications in the secondary structure, marked by a notable increase of 60.25 % in β-turns, accompanied by reductions of 16.45 % in α-helices and 33.84 % in β-sheets. This was confirmed through analyses of disulfide bond content and FTIR. The outcomes of this study hold promise for enhancing the stability of emulsion formulations based on HBP, achieved by harnessing the complex formation between HBP and AA.

Eating Quality and In Vitro Digestibility of Brown Rice Improved by Ascorbic Acid Treatments

The effects of ascorbic acid treatment alone and in combination with degreasing or hydrothermal treatment on eating quality and in vitro digestibility of brown rice were explored for improving poor mouthfeel and low digestibility, and the improvement mechanism was investigated. The results indicated that the texture of cooked brown rice was significantly improved by degreasing combined with ascorbic acid hydrothermal treatment; the hardness and chewiness decreased to the level of polished rice; the stickiness increased three times of the cooked untreated brown rice; and the sensory score and in vitro digestibility were significantly enhanced from 68.20 and 61.37% to 83.70 and 79.53%, respectively. In addition, the relative crystallinity and water contact angle of treated brown rice were respectively reduced from 32.74% and 113.39° to 22.55% and 64.93°, and normal temperature water uptake significantly increased. Scanning electron microscope showed that the separation of starch granules occurred inside cooked brown rice grain obviously. The improvement of eating quality and in vitro digestibility of brown rice is conducive to enhancing the consumers acceptance and human health.

The Effect of Ascorbic Acid Treatment on The Quality Changes of Fresh-Cut Leek During Cold Storage

Çalışmada askorbik asit (AA) uygulamasının taze kesilmiş ‘Lincoln’ pırasa çeşidinin soğukta depolama boyunca kalitesi üzerine etkileri incelenmiştir. Optimum dönemde derimi yapılan pırasalar hızlı bir şekilde laboratuvara nakledilmiştir. Pırasalar zorlanmış hava ile (2 °C) 6 saat süreyle ön soğutma işlemine tabi tutulduktan sonra uygulamalar (kontrol, %1 ve %2 AA) için üç gruba ayrılmıştır. Ön soğutma işleminden sonra pırasalar serin ve steril koşullar altında 5-6 °C sıcaklıktaki çeşme suyuna birkaç kez daldırarak bahçe kaynaklı toz ve kalıntılar uzaklaştırılmıştır. Taze kesim işleminden sonra %1 ve %2 AA uygulanmış pırasa örnekleriyle kontrol grubu köpük kâselere yerleştirilerek üzeri streç filmle (16 µ) kaplanmıştır. Ambalajlanmış pırasalar 0±1 °C ve %90±5 oransal nemde 30 gün boyunca depolanmıştır. Depolama boyunca altı gün aralıklarla pırasalarda ağırlık kaybı (%), yalancı gövde sertliği (N), suda çözünebilir kuru madde (%), titre edilebilir asitlik (g 100 ml-1), solunum hızı (ml CO2/kg‐1 h‐1), yalancı gövde rengi ve duyusal özellikler belirlenmiştir. AA uygulamaları kontrole kıyasla taze kesilmiş pırasalarda ağırlık kayıplarını azaltmıştır. Depolama boyunca %2’lik doz daha etkili olmak üzere, AA uygulamaları yalancı gövde sertliğini kontrole göre daha iyi korumuştur. Soğukta depolama boyunca AA uygulamaları taze kesilmiş pırasaların TEA miktarını korumuş ve solunum hızını net bir şekilde baskılamıştır. AA uygulamaları kontrol örneklerine kıyasla depolama süresince pırasaların görsel kalitelerini daha iyi korumuştur. Sonuç olarak, AA uygulanmayan kontrol grubundaki pırasalar 0±1 °C ve % 90±5 oransal nemde 24 gün depolanabilirken, her iki AA (%1ve %2) uygulaması bu süreyi 30 güne kadar uzatmıştır. Ancak farklı doz ve uygulama şekilleri kullanılarak bu konuda daha detaylı çalışmalara ihtiyaç vardır.

Context dependent effects of ascorbic acid treatment in TET2 mutant myeloid neoplasia

Loss-of-function TET2 mutations (TET2MT) are common in myeloid neoplasia. TET2, a DNA dioxygenase, requires 2-oxoglutarate and Fe(II) to oxidize 5-methylcytosine. TET2MT thus result in hypermethylation and transcriptional repression. Ascorbic acid (AA) increases dioxygenase activity by facilitating Fe(III)/Fe(II) redox reaction and may alleviate some biological consequences of TET2MT by restoring dioxygenase activity. Here, we report the utility of AA in the prevention of TET2MT myeloid neoplasia (MN), clarify the mechanistic underpinning of the TET2-AA interactions, and demonstrate that the ability of AA to restore TET2 activity in cells depends on N- and C-terminal lysine acetylation and nature of TET2MT. Consequently, pharmacologic modulation of acetyltransferases and histone deacetylases may regulate TET dioxygenase-dependent AA effects. Thus, our study highlights the contribution of factors that may enhance or attenuate AA effects on TET2 and provides a rationale for novel therapeutic approaches including combinations of AA with class I/II HDAC inhibitor or sirtuin activators in TET2MT leukemia.

Ascorbic acid prevents chloroquine-induced toxicity in inner glial cells

Ototoxicity is a collateral effect of prolonged treatment with chloroquine which is a widely utilized as an anti-lupus and anti-malarial drug. Glial cells of inner ear are responsible for maintenance of neuronal cells homeostasis in auditory system. In the current study we have evaluated chloroquine-induced toxicity and protective effect of ascorbic acid treatment on Schwann glial cell cultures of inner ear. Glial cells were cultured from organ of Corti of mice cochlear structure. Purity of Schwann glial cell was confirmed by S100 protein staining. Cell viability was evaluated in control and cultures treated with different concentrations of chloroquine. Glutamate uptake and ROS production were measured by HPLC and DCFH-DA probe fluorescence, respectively. Results have shown that chloroquine treatment evoked concentration and time -dependent toxicity (LC50 = 70 μM) as well as significant decrease on glutamate uptake and high production of ROS in glial cell cultures. Co-treatment with ascorbic acid has prevented both chloroquine-induced ROS production and chloroquine toxicity on glial cell cultures. This pre-clinical study is the first one to demonstrate chloroquine-induced ROS production by glial cells of inner ear as well as the protective effect exerted by ascorbic acid on these cells.

Effects of ascorbic acid treatment on developmental alterations in calcium-binding proteins and gamma-aminobutyric acid transporter 1 in the cerebellum of lead-exposed rats during pregnancy and lactation.

In the present study, we investigated the effects of lead (Pb) and ascorbic acid co-administration on rat cerebellar development. Female rats were randomly divided into the following groups: control, Pb, and Pb plus ascorbic acid (PA) groups. From one week prior to mating, female rats were administered Pb (0.3% Pb acetate in drinking water) and ascorbic acid (100 mg/kg, oral intubation). The chemical administration was stopped on postnatal day 21 when the morphology of the offspring's cerebellum is similar to that of the adult brain. The blood Pb level was significantly increased following long-term Pb exposure. Ascorbic acid reduced Pb levels in the dams and offspring. Nissl staining demonstrated that the number of Purkinje cells was significantly reduced following Pb exposure, while ascorbic acid ameliorated this effect in the cerebellum of the offspring. Calcium-binding proteins, such as calbindin, calretinin, and parvalbumin were commonly expressed in Purkinje cells, and Pb exposure and ascorbic acid treatment resulted in similar patterns of change, namely Pb-induced impairment and ascorbic acid-mediated amelioration. The gamma-aminobutyric acid transporter 1 (GABAT1) is expressed in the pinceau structure where the somata of Purkinje cells are entwined in inhibitory synapses. The number of GABAT1-immunoreactive synapses was reduced following Pb exposure, and ascorbic acid co-treatment prevented this effect in the cerebellar cortex. Therefore, it can be concluded that ascorbic acid supplementation to mothers during gestation and lactation may have potential preventive effects against Pb-induced impairments in the developing cerebellum via protection of inhibitory neurons and synapses.

Local treatment with ascorbic acid accelerates recovery of post-sutured Achilles tendon in male Wistar rats.

Tendon rupture is a very frequent accident involving average people and high-performance athletes. Clinical studies describe tendon recovery as a painful and slow process involving different biochemical and histological events. Ascorbic acid (AA) is a potent antioxidant as well as an important cofactor for collagen synthesis. In the current study, we evaluated if local treatment with AA is able to promote tendon repair in tenotomized rats. Animals were submitted to Achilles tendon rupture followed by surgical suture. Control and AA groups received in loco injection of saline solution (0.9% NaCl) and 30 mM AA, respectively. Histological and functional recovery of Achilles tendon tissue was evaluated at 7, 14, and 21 days post-surgery. Hematoxylin/eosin staining and collagen fluorescence analysis showed intense disarrangement of tendon tissue in the saline group. Tenotomized animals also showed hypercellularity in tendon tissue compared with non-tenotomized animals. The Achilles functional index (AFI) showed a significant decrease of tendon functionality in tenotomized animals at 7, 14, and 21 days post-surgery. AA accelerated tissue organization and the recovery of function of the Achilles tendons. The beneficial effect of AA treatment was also observed in the organization of the collagen network. Data presented in the current work showed that in loco treatment with AA accelerated the recovery of injured Achilles tendon post-surgery.

Mitigation of glyphosate-based herbicide toxicity in maize (Zea mays L.) seedlings by ascorbic acid

The toxicity of glyphosate at 3.6 mg L−1 to maize seedlings raised from un-treated seeds and the effectiveness of seed pretreatment by soaking in 0.25 mmol L−1 ascorbic acid (AsA) solution for mitigation of toxicity were evaluated in hydroponic culture. Glyphosate dramatically reduced the growth of roots and photosynthetic pigments in the leaves but increased protein content in the leaves. Superoxide dismutase activity and AsA concentration in the roots were increased, and guaiacol peroxidase (GPOX) activity was unaffected. Pretreatment with AsA improved the dry mass of the roots and shoots, increased the protein content in roots and leaves, and significantly decreased the activity of GPOX in roots. The positive effect of AsA treatment was not associated with more efficient functioning of the antioxidative system.

High-dose ascorbic acid induces carcinostatic effects through hydrogen peroxide and superoxide anion radical generation-induced cell death and growth arrest in human tongue carcinoma cells

High-dose ascorbic acid (AsA) treatment, known as pharmacological AsA, has been shown to exert carcinostatic effects in many types of cancer cells and in vivo tumour models. Although pharmacological AsA has potential as a complementary and alternative medicine for anticancer treatment, its effects on human tongue carcinoma have not yet been elucidated. In this study, we investigated the effect of AsA treatment on human tongue carcinoma HSC-4 cells compared with non-tumourigenic tongue epithelial dysplastic oral keratinocyte (DOK) cells. Our results show that treatment with 1 and 3 mM of AsA for 60 min preferentially inhibits the growth of human tongue carcinoma HSC-4 over DOK cells. Furthermore, AsA-induced effects were accompanied by increased intracellular oxidative stress and were repressed by treatment with a hydrogen peroxide (H2O2) scavenger catalase and a superoxide anion radical (O2−) scavenger, tempol. Time-lapse observation and thymidine analog EdU incorporation revealed that AsA treatment induces not only cell death but also suppression of DNA synthesis and cell growth. Moreover, the growth arrest was accompanied by abnormal cellular morphologies whereby cells extended dendrite-like pseudopodia. Taken together, our results demonstrate that AsA treatment can induce carcinostatic effects through induction of cell death, growth arrest, and morphological changes mediated by H2O2 and O2− generation. These findings suggest that high-dose AsA treatment represents an effective treatment for tongue cancer as well as for other types of cancer cells.

Effect of ascorbic acid treatment on some quality parameters of frozen strawberry and raspberry fruits

Abstract Strawberry (Red Dream and Camarosa varieties) and raspberry (Nova and Killarney varieties) fruits were harvested in the middle summer in eastern part of Georgia. After harvesting average samples were immediately dipped into 0%, 1% or 2% ascorbic acid solution at 20 ± 1 °C temperature with exposure time of 2.5 min. Then, the samples were frozen at −40 °C and stored in plastic containers at −20 °C for 6 months. After 3 months storage period Total soluble solids (TSS) of strawberry and raspberry fruits decreased by 10–14% in both treated and untreated samples. TSS changes in the next three months were not statistically significant. pH values of the samples also decreased by 10–13% after 3 months regardless treatment with ascorbic acid. In the next three months pH values continued decreasing approximately with the same rate for all the samples. Due to the treatment of the fruit samples by 1% and 2% ascorbic acid, content of the last one in fruits after three months storage was increased approximately by 30% and 100% respectively and was kept practically at the same level for the next six months. In the untreated fruits of Red Dream and Camarosa of strawberry varieties during the first three months storage Total phenolic compounds (TPC) reduced by 20%. In both untreated varieties of raspberry TPC reduced by 14%. Ascorbic acid treatment increased polyphenol retaining in all frozen samples of strawberry and raspberry fruits. For Camarosa treated with 2% ascorbic acid this effect was the highest – 15%; for Red Dream the effect was the lowest – 5%. The next three months storage practically did not affect TPC in Red Dream variety of strawberry fruits neither untreated nor treated ones. In the rest varieties of berries TPC decreased maximum by 29% (Camarosa 2% treated) and minimum by 9% (Nova untreated). Antioxidant potential of the fruits was in good correlation (R2 = 0.93) with TPC for all six months of storage.

Ascorbic acid inhibits TPA-induced HL-60 cell differentiation by decreasing cellular H₂O₂ and ERK phosphorylation.

Retinoic acid (RA), vitamin D and 12-O‑tetradecanoyl phorbol-13-acetate (TPA) can induce HL-60 cells to differentiate into granulocytes, monocytes and macrophages, respectively. Similar to RA and vitamin D, ascorbic acid also belongs to the vitamin family. High‑dose ascorbic acid (>100 µM) induces HL‑60 cell apoptosis and induces a small fraction of HL‑60 cells to express the granulocyte marker, CD66b. In addition, ascorbic acid exerts an anti‑oxidative stress function. Oxidative stress is required for HL‑60 cell differentiation following treatment with TPA, however, the effect of ascorbic acid on HL‑60 cell differentiation in combination with TPA treatment remains to be fully elucidated. The aim of the present study was to investigate the cellular effects of ascorbic acid treatment on TPA-differentiated HL-60 cells. TPA-differentiated HL-60 cells were used for this investigation, this study and the levels of cellular hydrogen peroxide (H2O2), caspase activity and ERK phosphorylation were determined following combined treatment with TPA and ascorbic acid. The results demonstrated that low‑dose ascorbic acid (5 µM) reduced the cellular levels of H2O2 and inhibited the differentiation of HL‑60 cells into macrophages following treatment with TPA. In addition, the results of the present study further demonstrated that low‑dose ascorbic acid inactivates the ERK phosphorylation pathway, which inhibited HL‑60 cell differentiation following treatment with TPA.

Senescence-induced increases in intracellular oxidative stress and enhancement of the need for ascorbic acid in human fibroblasts

Many studies have suggested that there is a close correlation among declines in internal ascorbic acid (AsA) levels, various disorders, and senescence. To clarify the relationships between age-associated changes in intracellular AsA levels and the effects of AsA administration on intracellular reactive oxygen species (ROS) levels, we investigated aging-related changes in AsA uptake, ROS levels, and the effects of AsA administration on intracellular ROS levels in young and old (senescent) human fibroblasts. Our results demonstrated that AsA uptake was increased in old cells compared with young cells, although mRNA and protein expression of sodium-dependent vitamin C transporter 2 was barely altered between the young and old cells. We also demonstrated that the intracellular superoxide anion level was higher in young cells, whereas the level of intracellular peroxides was significantly increased in old cells under both normal and oxidative stress conditions. Moreover, AsA administration markedly decreased the augmentation of intracellular peroxides in old cells, whereas there was no effect of AsA treatment in young cells under both normal and oxidative stress conditions. Therefore, our results also indicate that AsA could play an important role in regulating the intracellular ROS levels in senescent cells and that the need for AsA is enhanced by cellular senescence.

The Effect of Ascorbic Acid Treatment on Viability and Vigor Maize (Zea mays L.) Seedling under Drought Stress

This study was conducted in the laboratory and the field to examine the effects of ascorbic acid treatment on germination and seedling growth under drought stress. The laboratory works consisted of two experiments and were designed to determine the critical osmotic potential of maize and to determine the optimum ascorbic acid concentration. The field study was designed to examine the effects of soaking seed in ascorbic acid on seedling growth under drought stress. Drought condition was simulated by PEG-6000 and regulation of water treatment. During the first experiment, interactions of both osmotic potential and varieties were significant at all variables. Germination percentage and speed of germination were significantly decreased by increasing of osmotic potential. The second experiment showed that interactions of both factors were significant at all variables except vigor index, the length of shoot, primary, and seminal root. The results showed that the ascorbic acid treatment improved the germination percentage, the speed of germination and the vigor index compared with the control, besides the increase in length of shoot, primary and seminal root and number of seminal root. However, the best result was showed by 55 mM ascorbic acid. The result of field experiment showed that interactions were not always significant and 55 mM ascorbic acid treatment increased the seedling height, the number of leaves and leaf area but it had no effect on the water deficit and the root length.

Effects of Ascorbic Acid Treatment to Grapevine Rootstock-1616C and Vitis vinifera L. cvs. Razaki

Effects of Ascorbic Acid Treatment to Grapevine Rootstock-1616C and Vitis vinifera L. cvs. Razaki

Ascorbic Acid Transported by Sodium-Dependent Vitamin C Transporter 2 Stimulates Steroidogenesis in Human Choriocarcinoma Cells

Reduced vitamin C [ascorbic acid (AA)], which is taken up into cells by sodium-dependent vitamin C transporter (SVCT) 1 and 2, is believed to be important for hormone synthesis, but its role in generating placental steroids needed to maintain pregnancy and fetal development is not clear. To determine the steroidogenic effect of AA and the role of SVCT2 in AA-induced steroidogenesis, we tested the effects of AA treatment and SVCT2 knockdown on steroidogenesis in human choriocarcinoma cell lines. AA treatment of JEG-3, BeWo, and JAR cells for 48-h dose dependently increased progesterone and estradiol levels. In JEG-3 cells, AA increased the mRNA expression of P450 cholesterol side-chain cleavage enzyme, 3beta-hydroxysteroid dehydrogenase type 1, and aromatase, key enzymes for steroidogenesis. Stable knockdown of SVCT2 in JEG-3 cells by retrovirally mediated RNA interference decreased the maximal velocity of AA uptake by approximately 50%, but apparent affinity values were not affected. SVCT2 knockdown in JEG-3 cells significantly suppressed the AA-induced mRNA expression of placental P450 cholesterol side-chain cleavage enzyme, 3beta-hydroxysteroid dehydrogenase type 1, and aromatase. This suppression of the AA-induced mRNA expression of steroidogenic enzymes subsequently decreased progesterone and estradiol production. In addition, inhibition of MAPK kinase-ERK signaling, which is a major pathway for AA-regulated gene expression, failed to affect AA-induced steroidogenesis. Our observations indicate that SVCT2-mediated AA uptake into cells is necessary for AA-induced steroidogenesis in human choriocarcinoma cell, but MAPK kinase-ERK signaling is not involved in AA-induced steroidogenesis.

Inhibition of core browning in ‘Yali’ pear fruit by post-harvest treatment with ascorbic acid

Summary‘Yali’ pear fruit (Pyrus bretschneideri Rehd.) were treated after harvest by vacuum infiltration (–50 kN m–2) at 25ºC with ascorbic acid (AsA) at concentrations of 0.1 mM, 1.0 mM, or 10.0 mM for 5 min, or with distilled water (control) under the same conditions. Thereafter, fruit were placed in air storage at 12ºC and cooled to 0ºC over 30 d, then held at 0ºC and 80 – 90% relative humidity (RH) for a further 150 d.The core browning index (CBI) was reduced by 10.4%, 24.5% or 40.0% in ‘Yali’ pears treated with 0.1, 1.0 or 10.0 mM AsA, respectively, after 180 d of storage. The firmness and total soluble solids (TSS) content of fruit treated with 10.0 mM AsA were also higher than those of control fruit. AsA treatment had an inhibitory effect on the accumulation of malondialdehyde and H2O2. Moreover, AsA treatment effectively delayed the decline in AsA and glutathione levels, and maintained the activities of superoxide dismutase, catalase and ascorbate peroxidase. These results suggest that the effects of AsA treatment on inhibiting core browning and improving post-harvest quality in ‘Yali’ pears might be due to reducing membrane lipid peroxidation by enhancing the capacity of cells to scavenge reactive oxygen species.

Effect of ascorbic acid treatment on endothelium‐dependent and neurogenic relaxation of corpus cavernosum from middle‐aged non‐insulin dependent diabetic rats

The purpose of the present study was to investigate functional responses and nitric oxide synthase activity in the corpus cavernosum of young control, middle-aged control and middle-aged non-insulin dependent diabetic rats. The animal groups were treated with ascorbic acid. Acetylcholine-mediated endothelium-dependent relaxation of cavernosal tissue was significantly attenuated from a maximum of 58.0 +/- 4.1% (1 mmol, n = 10) in young rats to 44.3 +/- 1.6% in aged-matched controls (P < 0.05) and to 23.3 +/- 2.8% in non-insulin-dependent diabetes mellitus rats (P < 0.01). These deficits in acetylcholine responsiveness were completely prevented by ascorbic acid treatment. Non-adrenergic non-cholinergic relaxations evoked by electrical field stimulation (0.5-64.0 Hz) in the corpus cavernosum of middle-aged control and non-insulin dependent (NID) diabetic rats are blunted and were not restored by ascorbic acid. The histochemical findings demonstrated a decrease of nicotinamide adenine dinucleotide phosphate-diaphorase staining in the cavernosal tissue obtained from middle-aged control rats and middle-aged diabetic rats. Partial correction by ascorbic acid may suggest the importance of reactive oxygen species and a therapeutic approach in impotent NID diabetic men.

Intravenous iron preparations and ascorbic acid: Effects on chelatable and bioavailable iron

There is growing interest to use ascorbic acid as adjuvant therapy for patients with recombinant human erythropoietin-hyporesponsiveness (rHuEpo). Several clinical studies showed the beneficial effect of ascorbic acid treatment on hematologic parameters in rHuEpo-treated hemodialysis patients with elevated or even normal iron stores. However, whether ascorbic acid directly affects stability and cellular metabolism of intravenous iron preparations (IVI) is not well understood. The preparations for testing were iron sucrose (Venofer), ferric gluconate (Ferrlecit), and iron dextran (INFeD). HepG2-cells were used to investigate effects of ascorbic acid on iron bioavailability for the intracellular labile iron pool (LIP) from IVI by using the fluorescent calcein-assay, and cellular ferritin content was measured by enzyme-linked immunosorbent assay (ELISA). Transferrin-chelatable iron was assessed by fluorescent-apotransferrin, and cell toxicity was assayed by neutral red cytotoxicity test. The effects of vitamin C on different preparations do not reflect their known chemical stability (i.e., iron dextran >iron sucrose >ferric gluconate). Effects of ascorbic acid on the increase of the intracellular LIP, as well as on increasing mobilization to transferrin in serum, were limited to iron sucrose. Ascorbic acid did not increase cell toxicity and the amount of low molecular weight iron in serum. We conclude that corrected ascorbic acid levels in hemodialysis (HD) patients could increase the amount of bioavailable iron from iron sucrose, but not from other classes of IVI. Vitamin C administration could therefore result in a lower need of iron sucrose to correct anemia.

Development of lipid oxidation and flesh colour in frozen stored fillets of Norwegian spring-spawning herring ( Clupea harengus L.). Effects of treatment with ascorbic acid

Frozen stored fillets from Norwegian spring spawning herring ( Clupea harengus L.) become discoloured. Based on the hypothesis that lipid oxidation in the fillets caused discoloration, we designed an experiment where ascorbic acid was added to the water (2 g l −1) in RSW-tanks on board a fishing vessel and/or by spray (20 g l −1) after filleting but before freezing. Treatment with ascorbic acid on board and on the fillet line led to 8- and 17–24-fold increases, respectively, in the ascorbic acid concentration in the herring fillets. Ascorbic acid treatment on the fillet line, but not the treatment on board, protected the herring fillets against oxidation during freezing, an effect that could be detected until 9 weeks of storage at −30 °C. Between 9 and 14 weeks of storage there was a new burst of lipid oxidation where the treatments had no effect. There was a large variation in colour within each fillet and between fillets in the same group. During freezing, the amount of yellow colour increased substantially and the amount of red colour increased in the posterior end of the fillets, causing a visible change in appearance. Thereafter only minor changes occurred until week 10 but, in week 30, the fillets had become less red, causing a less fresh and more grey appearance. Compared to the within fillet and within group variations, there were only minor effects of ascorbic acid treatment on colour. It is suggested that shelf life of frozen herring fillets should be set at between 9 and 14 weeks at −30 °C. Treatment with ascorbic acid will not alleviate the discoloration of frozen herring fillets.

Evaluation of the effect of ascorbic acid treatment on wound healing in mice exposed to different doses of fractionated gamma radiation.

Alteration of the radiation-induced changes in wound contraction, collagen synthesis and wound histology by ascorbic acid was studied in mice exposed to 10, 16 and 20 Gy of fractionated (2 Gy/fraction) gamma radiation. The animals were given double-distilled water or ascorbic acid daily before exposure to 2 Gy/day of fractionated irradiation. A full-thickness skin wound was created on the dorsum of the irradiated mice, and the progression of wound contraction and collagen synthesis were examined and histological evaluations were carried out at various times after wounding. Irradiation caused a dose-dependent delay in wound contraction, and pretreatment with ascorbic acid resulted in a significant increase in wound contraction. The greatest increase in wound contraction was observed 6 and 9 days after wounding in both groups. Pretreatment with ascorbic acid augmented the synthesis of collagen significantly as revealed by an increase in hydroxyproline content. The collagen deposition and fibroblast and vasculature densities declined in a dose-dependent manner in groups receiving radiation alone as indicated by histological evaluation. Pretreatment with ascorbic acid ameliorated the observed effect significantly. These studies demonstrate that pretreatment with ascorbic acid resulted in a significant reduction of radiation-induced delay in wound healing as shown by earlier wound closure and increased collagen content and fibroblast and vascular densities.