Genotoxic effects of electromagnetic field radiations from mobile phones.

The use of wireless communication technology in mobile phones has revolutionized modern telecommunication and mobile phones have become so popular that their number exceeds the global population. Electromagnetic field radiations (EMR) are an integral part of wireless technology, which are emitted by mobile phones, mobile tower antennas, electric power stations, transmission lines, radars, microwave ovens, television sets, refrigerators, diagnostic, therapeutic, and other electronic devices. Manmade EMR sources have added to the existing burden of natural EMR human exposure arising from the Sun, cosmos, atmospheric discharges, and thunder storms. EMR including radiofrequency waves (RF) and extremely low-frequency radiation (ELF) has generated great interest as their short-term exposure causes headache, fatigue, tinnitus, concentration problems, depression, memory loss, skin irritation, sleep disorders, nausea, cardiovascular effects, chest pain, immunity, and hormonal disorders in humans, whereas long-term exposure to EMR leads to the development of cancer. The review has been written by collecting the information using various search engines including google scholar, PubMed, SciFinder, Science direct, EMF-portal, saferemr, and other websites from the internet. The main focus of this review is to delineate the mutagenic and genotoxic effects of EMR in humans and mammals. Numerous investigations revealed that exposure in the range of 0-300 GHz EMR is harmless as it did not increase micronuclei and chromosome aberrations. On the contrary, several other studies have demonstrated that exposure to EMR is genotoxic and mutagenic as it increases the frequency of micronuclei, chromosome aberrations, DNA adducts, DNA single and double strand breaks at the molecular level in vitro and in vivo. The EMR exposure induces reactive oxygen species and changes the fidelity of genes involved in signal transduction, cytoskeleton formation, and cellular metabolism.

NF-κB and COX-2 repression with topical application of hesperidin and naringin hydrogels augments repair and regeneration of deep dermal wounds.

INTRODUCTION: Wound injury is common and causes serious complications if not treated properly. The moist dressing heals wounds faster than other dressings. Therefore, we sought to study the effect of hesperidin/naringin hydrogel wound dressing or their combinations on the deep dermal wounds in mice. METHODS: A rectangular full thickness skin flap of 2.5 × 1.5 cm was excised from depilated mice dorsum and the wound was fully covered with 5% hesperidin/5% naringin hydrogel or both in the ratio of 1:1, 2:1, or 1:2, respectively once daily until complete healing of the wound. Data were collected on wound contraction, mean wound healing time, collagen, DNA, and nitric oxide syntheses, glutathione concentration, superoxide dismutase activity, and lipid peroxidation throughout healing. Expression of NF-κB and COX-2 were also estimated in the regenerating granulation tissue using Western blot. FINDINGS: Dressing of wounds with 5% hesperidin hydrogel led to a higher and early wound contraction and significantly reduced mean wound healing time by 5.7 days than 5% naringin or combination of hesperidin and naringin hydrogels in the ratio of 1:1, 2:1, or 1:2. Hesperidin hydrogel wound dressing caused higher collagen and DNA syntheses than other groups at all times after injury. Glutathione concentration and superoxide dismutase activity increased followed by a decline in lipid peroxidation in regenerating wounds after hesperidin/naringin hydrogel application and a maximum effect was observed for hesperidin alone. The hesperidin/naringin hydrogel suppressed NF-κB and COX-2 expression on days 6 and 12. CONCLUSIONS: Application of 5% hesperidin hydrogel was more effective than 5% naringin or combination of hesperidin and naringin gels (1:1, 2:1 or 1:2) indicated by a greater wound contraction, reduced mean wound healing time, elevated collagen and DNA syntheses, rise in glutathione concentration, and superoxide dismutase activity followed by reduced lipid peroxidation, and NF-κB, and COX-2 expression.

Sonapatha (Oroxylum indicum) mediates cytotoxicity in cultured HeLa cells by inducing apoptosis and suppressing NF-κB, COX-2, RASSF7 and NRF2.

Oroxylum indicum (Sonapatha) is traditionally used to cure several human ailments. Therefore, the cell killing effect of chloroform, ethanol, and water extracts of Sonapatha was studied in cultured HeLa cells treated with 0-100 µg/mL of these extracts/doxorubicin by MTT assay. Since ethanol extract was most cytotoxic its effect was further investigated by clonogenic, apoptosis, necrosis, and lactate dehydrogenase assays. The mechanism of cytotoxicity of Sonapatha was determined at the molecular level by estimation of caspase 8 and 3 activities and Western blot analysis of NF-κB, COX-2, Nrf2, and RASSF7 which are overexpressed in neoplastic cells. HeLa cells treated with Sonapatha extract exhibited a concentration and time-dependent rise in the cytotoxicity as indicated by the MTT assay. Ethanol extract of Sonapatha (0, 20, 40, and 80 µg/mL) reduced clonogenicity, increased DNA fragmentation, apoptotic and necrotic indices, lactate dehydrogenase release, caspase 8 and 3 activities and inhibited the overexpression of NF-κB, COX-2, Nrf2, and RASSF7 in HeLa cells concentration-dependently.

Antioxidant activity of curcumin protects against the radiation-induced micronuclei formation in cultured human peripheral blood lymphocytes exposed to various doses of γ-Radiation.

PURPOSE: Ionizing radiations trigger the formation of free radicals that damage DNA and cause cell death. DNA damage may be simply evaluated by micronucleus assay and the pharmacophores that impede free radicals could effectively reduce the DNA damage initiated by irradiation. Therefore, it was desired to determine the capacity of curcumin to alleviate micronuclei formation in human peripheral blood lymphocytes (HPBLs) exposed to 0-4 Gy of γ-radiation. MATERIALS AND METHODS: HPBLs were exposed to 3 Gy after 30 minutes of 0.125, 0.25, 0.5, 1, 2, 5, 10, 20 or 50 µg/mL curcumin treatment or with 0.5 µg/mL curcumin 30 minutes early to 0, 0.5, 1, 2, 3 or 4 Gy 60Co γ-irradiation. Cytokinesis of HPBLs was blocked by cytochalasin B and micronuclei scored. The ability of curcumin to suppress free radical induction in vitro was determined by standard methods. RESULTS: HPBLs treated with different concentrations of curcumin before 3 Gy irradiation alleviated the micronuclei formation depending on curcumin concentration and the lowest micronuclei were detected at 0.5 µg/mL curcumin when compared to 3 Gy irradiation alone. Increasing curcumin concentration caused a gradual rise in micronuclei, and the significant increases were detected at 10-50 µg/mL curcumin than 3 Gy irradiation alone. Irradiation of HPBLs to different doses of γ-rays caused a significant rise in micronuclei depending on radiation dose, whereas HPBLs treated with 0.5 µg/mL curcumin 30 minutes before irradiation to different doses of γ-rays significantly reduced frequencies of HPBLs with one, two, or more micronuclei. Curcumin treatment inhibited the formation of hydroxyl (OH), 2,2-azinobis(3-ethylbenzothiazoline-6-sulfonic acid (ABTS), 2,2'-diphenyl-1-picrylhydrazyl (DPPH), and (nitric oxide) NO free radicals in a concentration-related way. CONCLUSIONS: Curcumin when treated at a dose of 0.5 µg/mL attenuated micronuclei formation after γ-irradiation by inhibiting the formation of radiation-induced free radicals.

(E)4-[4-N,N-dimethylaminophenyl]but-3-en-2-one mitigates radiation-induced chromosome damage in BALB/c mouse bone marrow.

We examined the effects of administration of (E) 4-[4-N,N-dimethylaminophenyl]but-3-en-2-one (DMAP) on radiation-induced chromosome damage in mice. Mice were whole-body exposed to γ-rays, 0-4 Gy, and then immediately administered DMAP, 20 mg/kg. After 24 h, mice were sacrificed, femora were removed, marrow was extracted, and chromosome aberrations were scored in the bone marrow cells. With vehicle-only (saline or oil) treatment, radiation dose-dependent damage was seen in aberrant cells, chromosome breaks, chromatid breaks, centric rings, di-, tri-, and tetracentrics, acentric fragments, total aberrations, polyploidy, and pulverization. Post-administration of DMAP was protective as it reduced chromosome damage. DMAP treatment may be a useful protective agent following radiation accidents or radiotherapy.

Chemopreventive effect of hesperidin, a citrus bioflavonoid in two stage skin carcinogenesis in Swiss albino mice.

The cancer-protective ability of hesperidin was investigated on 7, 12-dimethylbenz[a]anthracene (DMBA) and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced skin carcinogenesis in Swiss albino mice. Topical application of DMBA+TPA on mice skin led to 100% tumour incidence and rise in average number of tumours. Administration of different doses of hesperidin (HPD) before (pre) or after (post) and continuous (pre and post) DMBA application significantly reduced tumour incidence and average number of tumours in comparison to DMBA+TPA treatment alone. Topical application of DMBA+TPA increased oxidative stress as shown by significantly increased TBARS values and reduced glutathione contents, and glutathione-S-transferase, superoxide dismutase and catalase activities. Hesperidin treatment significantly reduced TBARS values and elevated glutathione concentration and glutathione-S-transferase, superoxide dismutase and catalase activities in the skin/tumors of mice treated with HPD+DMBA+TPA, HPD+DMBA+TPA+HPD or DMBA+TPA+HPD when compared to DMBA+TPA application alone. The study of molecular mechanisms showed that hesperidin suppressed expression of Rassf7, Nrf2, PARP and NF-κB in a dose dependent manner with a maximum inhibition at the level of 300 mg/kg body weight hesperidin. In conclusion, oral administration of hesperidin protected mice against chemical carcinogenesis by increasing antioxidant status, reducing DMBA+TPA induced lipid peroxidation and inflammatory response, and repressing of Rassf7, Nrf2, PARP and NF-κB levels.

Chronic low dose exposure of hospital workers to ionizing radiation leads to increased micronuclei frequency and reduced antioxidants in their peripheral blood lymphocytes.

Purpose: The regular low dose occupational exposure to ionizing radiation may induce deleterious health effects, which may be of particular interest to medical radiation workers who daily handle X-ray machines. Human peripheral blood lymphocytes are able to retain the signature of radiation-induced DNA damage, therefore, the present study was undertaken to investigate the DNA damage and antioxidants status in hospital workers occupationally exposed to low doses of X-rays. Materials and methods: The peripheral blood lymphocytes of the occupationally exposed and control groups matched for age, gender, tobacco usage, and alcohol consumption were cultured and micronuclei frequency was determined. Activities of antioxidant enzymes and lipid peroxidation were also estimated in their plasma. Results: The micronuclei frequency in the occupationally exposed group (n = 33), increased significantly (p < .0001) followed by reduced glutathione-s-transferase (p < .01) and catalase (p < .001) activities, and increased lipid peroxidation (p < .05) when compared to the control group (n = 33). Occupational exposure resulted in an effective dose ranging between 3.14 to 144.5 mSv (40.88 ± 39.86mSv) depending on the employment duration of 3-29 years (10.33 ± 7.05 years). A correlation between the micronuclei frequency (p < .05) and catalase activity (p < .05) existed in the occupationally exposed individuals depending on the smoking habit, age, duration of employment, cumulative exposure dose and number of patients handled per day. Conclusions: We have observed that protracted low dose exposure to ionizing radiation is an inevitable occupational hazard leading to persistence of oxidative stress and increased genomic instability in the radiological technicians depending on the time spent with X-rays, cumulative dose received and the number of patients handled daily raising the risk of cancer development.

Topical application of stem bark ethanol extract of Sonapatha, Oroxylum indicum (L.) Kurz accelerates healing of deep dermal excision wound in Swiss albino mice.

ETHNOPHARMACOLOGICAL RELEVANCE: The Oroxylum indicum is used traditionally to treat fever, colic, stomach ulcers, constipation, indigestion, intestinal worms, strangury, asthma, cough, hiccough, diarrhea, dysentery and wounds by the herbal healers of Mizoram and it is also part of Ayurvedic formulations. AIMS OF THE STUDY: The wound healing activity of Oroxylum indicum has not been investigated. Therefore, the present study was undertaken to evaluate the ability of different concentrations of ethanol extract of stem bark of Oroxylum indicum in the deep dermal excision wounds of mice. MATERIALS AND METHODS: The deep dermal excision wound was created on the shaved dorsum of Swiss albino mice. Each excision wound was topically applied with 5%, 10%, 20% or 30% gel of stem bark ethanol extract of Oroxylum indicum (OIE) and wound contraction, mean wound healing time (MHT), collagen and DNA syntheses were studied. The expression of NF-κB and COX-II were evaluated in the regenerating wound granulation tissues of mice. RESULTS: Topical application of different concentrations of OIE resulted in a concentration dependent rise in wound contraction and MHT and the highest wound contraction was recorded for 10% OIE. Similarly, topical application of different concentrations of OIE increased the DNA and neocollagen syntheses in a dose dependent manner at all post wounding days and the greatest acceleration in DNA and neocollagen formation was observed for 10% OIE. The evaluation of lipid peroxidation (LOO) showed a dose dependent decline in LOO, which was lowest for 10% OIE. The study of molecular mechanisms revealed the suppression of NF-κB and COX-II in a dose dependent manner in the regenerating wound of mice with a maximum inhibition at 10% OIE. CONCLUSIONS: The present study demonstrates that OIE accelerated the wound contraction and reduced mean wound healing time in mice, which may be due to increased collagen and DNA syntheses, reduced lipid peroxidation coupled by NF-κB and COX-II suppression by OIE in the regenerating wounds of mice.

Evaluation of the free-radical scavenging and antioxidant activities of Chilauni, Schima wallichii Korth in vitro.

AIM: Free radicals are an outcome of various metabolic activities and their excess production leads to many diseases. Therefore, it is necessary to neutralize excess free radicals. MATERIALS & METHODS: Free-radical scavenging activity of various extracts of Schima wallichii was evaluated using standard protocols. RESULTS: Chloroform, ethanol and aqueous extracts of S. wallichii scavenged DPPH, hydroxyl, superoxide, nitric oxide and ABTS free radicals and increased ferric-reducing antioxidant potential in a concentration-dependent manner. A total of 1000 µg/ml of all the extracts and ethanol extract showed highest total flavonoids and phenol contents, respectively. CONCLUSION: The different extracts of S. wallichii scavenged different free radicals efficiently due to the presence of flavonoids and polyphenols and may be helpful in free radical-induced diseases.

Impact of radiofrequency radiation on DNA damage and antioxidants in peripheral blood lymphocytes of humans residing in the vicinity of mobile phone base stations.

Radiofrequency radiations (RFRs) emitted by mobile phone base stations have raised concerns on its adverse impact on humans residing in the vicinity of mobile phone base stations. Therefore, the present study was envisaged to evaluate the effect of RFR on the DNA damage and antioxidant status in cultured human peripheral blood lymphocytes (HPBLs) of individuals residing in the vicinity of mobile phone base stations and comparing it with healthy controls. The study groups matched for various demographic data including age, gender, dietary pattern, smoking habit, alcohol consumption, duration of mobile phone use and average daily mobile phone use. The RF power density of the exposed individuals was significantly higher (p < 0.0001) when compared to the control group. The HPBLs were cultured and the DNA damage was assessed by cytokinesis blocked micronucleus (MN) assay in the binucleate lymphocytes. The analyses of data from the exposed group (n = 40), residing within a perimeter of 80 m of mobile base stations, showed significantly (p < 0.0001) higher frequency of micronuclei when compared to the control group, residing 300 m away from the mobile base station/s. The analysis of various antioxidants in the plasma of exposed individuals revealed a significant attrition in glutathione (GSH) concentration (p < 0.01), activities of catalase (CAT) (p < 0.001) and superoxide dismutase (SOD) (p < 0.001) and rise in lipid peroxidation (LOO) when compared to controls. Multiple linear regression analyses revealed a significant association among reduced GSH concentration (p < 0.05), CAT (p < 0.001) and SOD (p < 0.001) activities and elevated MN frequency (p < 0.001) and LOO (p < 0.001) with increasing RF power density.

Investigation of the Anti-Inflammatory and Analgesic Activities of Ethanol Extract of Stem Bark of Sonapatha Oroxylum indicum In Vivo.

Inflammation is all a pervasive phenomenon, which is elicited by the body in response to obnoxious stimuli as a protective measure. However, sustained inflammation leads to several diseases including cancer. Therefore it is necessary to neutralize inflammation. Sonapatha (Oroxylum indicum), a medicinal plant, is traditionally used as a medicine in Ayurveda and other folk systems of medicine. It is commonly used to treat inflammatory diseases including rheumatoid arthritis and asthma. Despite this fact its anti-inflammatory and analgesic effects are not evaluated scientifically. Therefore, the anti-inflammatory and analgesic activities of Sonapatha (Oroxylum indicum) were studied in Swiss albino mice by different methods. The hot plate, acetic acid, and tail immersion tests were used to evaluate the analgesic activity whereas xylene-induced ear edema and formalin induced paw edema tests were used to study the anti-inflammatory activity of Sonapatha. The administration of mice with 250 and 300 mg/kg b.wt. of O. indicum reduced pain and inflammation indicating that Sonapatha possesses analgesic and anti-inflammatory activities. The maximum analgesic and anti-inflammatory activities were observed in mice receiving 300 mg/kg b.wt. of O. indicum ethanol extract. Our study indicates that O. indicum possesses both anti-inflammatory and analgesic activities and it may be useful as an anti-inflammatory agent in the inflammation related disorders.

Curcumin Stimulates the Antioxidant Mechanisms in Mouse Skin Exposed to Fractionated γ-Irradiation.

Fractionated irradiation is one of the important radiotherapy regimens to treat different types of neoplasia. Despite of the immense therapeutic gains accrued by delivering fractionated irradiation to tumors, the radiation burden on skin increases significantly. Low doses of irradiation to skin adversely affect its molecular and metabolic status. The use of antioxidant/s may help to alleviate the radiation-induced changes in the skin and allow delivering a higher dose of radiation to attain better therapeutic gains. Curcumin is an antioxidant and a free radical scavenging dietary supplement, commonly used as a flavoring agent in curries. Therefore, the effect of 100 mg/kg body weight curcumin was studied on the antioxidant status of mice skin exposed to a total dose of 10, 20 and 40 Gy γ-radiation below the rib cage delivered as a single fraction of 2 Gy per day for 5, 10 or 20 days. Skin biopsies from both the curcumin treated or untreated irradiated groups were collected for the biochemical estimations at various post-irradiation times. The irradiation of animals caused a dose dependent decline in the glutathione concentration, glutathione peroxidase, and superoxide dismutase activities and increased the lipid peroxidation in the irradiated skin. Curcumin treatment before irradiation resulted in a significant rise in the glutathione concentration and activities of both the glutathione peroxidase and superoxide dismutase enzymes in mouse skin, whereas lipid peroxidation declined significantly. The present study indicates that curcumin treatment increased the antioxidant status of mouse exposed to different doses of fractionated γ-radiation.

Inhibition of radiation-induced DNA damage by jamun, Syzygium cumini, in the cultured splenocytes of mice exposed to different doses of γ-radiation.

The radioprotective property of 50 mg/kg body weight jamun (Syzygium cumini) extract was studied in the cultured splenocytes of mice exposed to 0, 0.5, 1, 2, 3, or 4 Gy of γ-radiation. The spleens of irradiated mice were removed aseptically and the splenocytes were extracted from the individual spleens and cultured. The micronuclei were prepared 72 hours after irradiation in binucleate splenocytes by blocking cytokinesis with cytochalasin-B. Irradiation of mice resulted in a dose-dependent elevation in the micronucleated splenocytes. The exposure of mice not only elevated splenocytes bearing one micronucleus but also cells bearing 2 and multiple (>2) micronuclei indicating induction of complex DNA damage after irradiation. Oral treatment of mice with 50 mg/kg body weight of jamun leaf extract protected against the radiation-induced micronuclei formation. Jamun extract also protected against the formation of 2 and multiple micronuclei indicating repair or inhibition of complex DNA damage. The assessment of lipid peroxidation in mice brain homogenate has indicated a concentration dependent inhibition of lipid peroxidation by jamun extract. Studies in a cell free system revealed that jamun extract inhibited the formation of OH, O(2)-, DPPH, and ABTS(+) free radicals in a concentration dependent manner. Our study demonstrates that jamun extract protected mice against the radiation-induced DNA damage and inhibition of radiation-induced free radical formation may be one of the mechanisms of radioprotection.

Acceleration of wound repair by curcumin in the excision wound of mice exposed to different doses of fractionated γ radiation.

Fractionated irradiation (IR) before or after surgery of malignant tumours causes a high frequency of wound healing complications. Our aim was to investigate the effect of curcumin (CUM) on the healing of deep excision wound of mice exposed to fractionated IR by mimicking clinical conditions. A full-thickness dermal excision wound was created on the shaved dorsum of mice that were orally administered or not with 100 mg of CUM per kilogram body weight before partial body exposure to 10, 20 or 40 Gy given as 2 Gy/day for 5, 10 or 20 days. The wound contraction was determined periodically by capturing video images of the wound from day 1 until complete healing of wounds. Fractionated IR caused a dose-dependent delay in the wound contraction and prolonged wound healing time, whereas CUM administration before fractionated IR caused a significant elevation in the wound contraction and reduced mean wound healing time. Fractionated IR reduced the synthesis of collagen, deoxyribonucleic acid (DNA) and nitric oxide (NO) at different post-IR times and treatment of mice with CUM before IR elevated the synthesis of collagen, DNA and NO significantly. Histological examination showed a reduction in the collagen deposition, fibroblast and vascular densities after fractionated IR, whereas CUM pre-treatment inhibited this decline significantly. Our study shows that CUM pre-treatment accelerated healing of irradiated wound and could be a substantial therapeutic strategy in the management of irradiated wounds.

Alleviation of iron induced oxidative stress by the grape fruit flavanone naringin in vitro.

Iron is an essential element that participates in several metabolic activities of cells; however, excess iron is a major cause of iron-induced oxidative stress and several human diseases. The protective effect of naringin, a grape fruit flavanone, was studied in iron overloaded isolated mouse liver mitochondria, where the isolated mitochondrial fraction was incubated with various concentrations of naringin before ferric ion loading. Iron overloading of mitochondrial fraction resulted in an increase in lipid peroxidation, protein oxidation, and DNA damage, whereas iron overload reduced the glutathione (GSH) concentration, glutathione-S-transferase (GST), glutathione peroxidase (GSHPx), catalase and superoxide dismutase (SOD) activities. Pretreatment of mitochondrial fraction with naringin inhibited iron-induced lipid peroxidation, protein oxidation, and DNA damage. Conversely, naringin supplementation arrested iron-induced depletion in the GSH contents, GSHPx, GST, SOD and catalase activities significantly. Ferric iron reduction assay revealed that naringin could not reduce ferric iron into ferrous iron indicating that it did not exhibit prooxidant activity. Iron free coordination site assay indicated that naringin was unable to occupy all the active sites of iron indicating that naringin did not completely chelate iron. Our study demonstrates that naringin was able to share the burden of endogenous oxidants by inhibiting the iron-induced depletion of all important antioxidant enzymes as well as GSH and may act as a good antioxidant.

Modulation of doxorubicin-induced genotoxicity by Aegle marmelos in mouse bone marrow: a micronucleus study.

The effect of various concentrations of Aegle marmelos (AME) on the doxorubicin (DOX)-induced genotoxic effects in mice bone marrow was studied. Treatment of mice with different concentrations of DOX resulted in a dose-dependent elevation in the frequency of micronucleated polychromatic (MPCE) as well as normochromatic (MNCE) erythrocytes in mouse bone marrow. The frequencies of MPCE and MNCE increased with scoring time, and the greatest elevation for MPCE was observed at 48 hours post-DOX treatment, whereas a maximum increase in MNCE was observed at 72 hours post-DOX treatment. This increase in MPCE and MNCE was accompanied by a decline in the polychromatic erythrocytes-normochromatic erythrocytes (PCE/NCE) ratio, which showed a DOX-dose-dependent decline. Treatment of mice with 200, 250, 300, 350, and 400 mg/kg body weight of AME, orally once daily for 5 consecutive days before DOX treatment, significantly reduced the frequency of DOX-induced micronuclei accompanied by a significant elevation in the PCE/NCE ratio at all scoring times. The greatest protection against DOX-induced genotoxicity was observed at 350 mg/kg AME. The protection against DOX-induced genotoxicity by AME may be due to inhibition of free radicals and increased antioxidant status.

"Spicing up" of the immune system by curcumin.

Curcumin (diferuloylmethane) is an orange-yellow component of turmeric (Curcuma longa), a spice often found in curry powder. Traditionally known for its an antiinflammatory effects, curcumin has been shown in the last two decades to be a potent immunomodulatory agent that can modulate the activation of T cells, B cells, macrophages, neutrophils, natural killer cells, and dendritic cells. Curcumin can also downregulate the expression of various proinflammatory cytokines including TNF, IL-1, IL-2, IL-6, IL-8, IL-12, and chemokines, most likely through inactivation of the transcription factor NF-kappaB. Interestingly, however, curcumin at low doses can also enhance antibody responses. This suggests that curcumin's reported beneficial effects in arthritis, allergy, asthma, atherosclerosis, heart disease, Alzheimer's disease, diabetes, and cancer might be due in part to its ability to modulate the immune system. Together, these findings warrant further consideration of curcumin as a therapy for immune disorders.

Ascorbic acid increases healing of excision wounds of mice whole body exposed to different doses of gamma-radiation.

Because of the practical importance of acute radiation exposure associated with combined injuries, it is imperative to investigate the efficacy of cost-effective nutritional factors in the reconstruction of irradiated wounds. Therefore, effect of pretreatment of ascorbic acid was studied on the healing of excised wounds in mice exposed to 2, 4, 6 and 8 Gy whole body gamma-radiation. A full-thickness wound was created on the dorsum of the irradiated mice and the progression of wound contraction was monitored by capturing video images of the wound at various varying days after irradiation. Irradiation caused a dose dependent delay in wound contraction and wound healing time, while ascorbic acid pretreatment resulted in a significant acceleration in the rate of wound contraction and a decrease in the mean wound healing time. To understand the mechanism of healing, collagen, hexosamine, DNA, nitrite and nitrate contents were measured in the granulation tissue of wounded mice treated with ascorbic acid before exposure to 6 Gy gamma-radiation. Ascorbic acid treatment prior to irradiation enhanced the synthesis of collagen, hexosamine, DNA, nitrite and nitrate contents. The histological assessment of wound biopsy revealed an improved collagen deposition, and increase in fibroblast and vascular densities. The present study demonstrates that ascorbic acid pretreatment has a beneficial effect on the irradiated wound and could be a substantial therapeutic strategy to accelerate wound repair in irradiated wounds and in the cases of combined injury situations.

Naringin, a grapefruit flavanone, protects V79 cells against the bleomycin-induced genotoxicity and decline in survival.

The effect of naringin, a grapefruit flavonone was studied on bleomycin-induced genomic damage and alteration in the survival of cultured V79 cells. Exposure of V79 cells to bleomycin induced a concentration dependent elevation in the frequency of binucleate cells bearing micronuclei (MNBNC) and a maximum number of MNBNCs were observed in the cells treated with 50 microg ml(-1) bleomycin, the highest concentration evaluated. This genotoxic effect of bleomycin was reflected in the cell survival, where a concentration dependent decline was observed in the cells treated with different concentrations of bleomycin. Treatment of cells with 1 mm naringin before exposure to different concentrations of bleomycin arrested the bleomycin-induced decline in the cell survival accompanied by a significant reduction in the frequency of micronuclei when compared with bleomycin treatment alone. The cell survival and micronuclei induction were found to be inversely correlated. The repair kinetics of DNA damage induced by bleomycin was evaluated by exposing the cells to 10 microg ml(-1) bleomycin using single cell gel electrophoresis. Treatment of V79 cells with bleomycin resulted in a continuous increase in DNA damage up to 6 h post-bleomycin treatment as evident by migration of more DNA into the tails (% tail DNA) of the comets and a subsequent increase in olive tail moment (OTM), an index of DNA damage. Treatment of V79 cells with 1 mm naringin reduced bleomycin-induced DNA damage and accelerated DNA repair as indicated by a reduction in % tail DNA and OTM with increasing assessment time. A maximum reduction in the DNA damage was observed at 6 h post-bleomycin treatment, where it was 5 times lower than bleomycin alone. Our study, which was conducted on the basis of antioxidant, free radical scavenging and metal chelating properties of naringin demonstrates that naringin reduced the genotoxic effects of bleomycin and consequently increased the cell survival and therefore may act as a chemoprotective agent in clinical situations.

Evaluation of Cytotoxic Effects of Dichloromethane Extract of Guduchi (Tinospora cordifolia Miers ex Hook F & THOMS) on Cultured HeLa Cells.

Extracts of Tinospora cordifolia (TCE) have been shown to possess anti-tumor properties, but the mechanism of the anti-tumor function of TCE is poorly understood. This investigation elucidates the possible mechanism underlying the cytotoxic effects of dichlormethane extracts of TCE, after selecting optimal duration and concentration for treatment. HeLa cells were exposed to various concentrations of TCE, which has resulted in a concentration-dependent decline in the clonogenicity, glutathione-S-transferase (GST) activity and a concentration-dependent increase in lipid peroxidation (TBARS) with a peak at 4 h and lactate dehydrogenase (LDH) release with a peak at 2 h. Our results suggest that the cytotoxic effect of TCE may be due to lipid peroxidation and release of LDH and decline in GST.