Indian Gooseberry and Barley Sprout Complex Prevent Oxidative Stress and Photoaging of the Skin in Ultraviolet B-Irradiated SHK-I Mice.

This study investigated the protective effects of a complex of Indian gooseberry and barley sprout (IB complex) on oxidative stress and skin damage caused by ultraviolet B irradiation in SHK-I hairless mice. The study examined the impact of IB complex on skin hydration, wrinkle formation, and melanogenesis using enzyme-linked immunosorbent assay, real-time polymerase chain reaction, and western blot analysis. The IB complex reduced skin hydration loss and wrinkle formation, while also demonstrating enhanced antioxidant activities. The IB complex maintained skin hydration via upregulation of hyaluronic acid and ceramide synthesis, including the regulation of hyaluronic acid synthase, long-chain ceramide formation, dihydroceramide desaturase 1 activity, and type I collagen production. The IB complex prevented wrinkle formation via downregulating JNK and upregulating TGF-ß pathways. Moreover, IB complex blocked melanin production via inhibition of protein kinase A, cAMP response element-binding protein, and microphthalmia-associated transcription factor pathways. These results suggest that IB complex is a potential agent to protect the skin against photodamage caused by exposure to UVB radiation. The research protocols underwent approval from the Institutional Animal Care and Use Committee of Kyung Hee University (KHGASP-21-577), ensuring compliance with ethical standards.

Ashwagandha Diminishes Hippocampal Apoptosis Induced by Microwave Radiation by Acetylcholinesterase Dependent Neuro-Inflammatory Pathway in Male Coturnix coturnix Japonica.

Microwave radiation (MWR) has been linked to neurodegeneration by inducing oxidative stress in the hippocampus of brain responsible for learning and memory. Ashwagandha (ASW), a medicinal plant is known to prevent neurodegeneration and promote neuronal health. This study investigated the effects of MWR and ASW on oxidative stress and cholinergic imbalance in the hippocampus of adult male Japanese quail. One control group received no treatment, the second group quails were exposed to MWR at 2 h/day for 30 days, third was administered with ASW root extract orally 100 mg/day/kg body weight and the fourth was exposed to MWR and also treated with ASW. The results showed that MWR increased serum corticosterone levels, disrupted cholinergic balance and induced neuro-inflammation. This neuro-inflammation further led to oxidative stress, as evidenced by decreased activity of antioxidant enzymes SOD, CAT and GSH. MWR also caused a significant decline in the nissil substances in the hippocampus region of brain indicating neurodegeneration through oxidative stress mediated hippocampal apoptosis. ASW, on the other hand, was able to effectively enhance the cholinergic balance and subsequently lower inflammation in hippocampus neurons. This suggests that ASW can protect against the neurodegenerative effects of MWR. ASW also reduced excessive ROS production by increasing the activity of ROS-scavenging enzymes. Additionally, ASW prevented neurodegeneration through decreased expression of caspase-3 and caspase-7 in hippocampus, thus promoting neuronal health. In conclusion, this study showed that MWR induces apoptosis and oxidative stress in the brain, while ASW reduces excessive ROS production, prevents neurodegeneration and promotes neuronal health.

Anti-radiation effect of MRN-100: a hydro-ferrate fluid, in vivo.

Ionizing radiation (IR) severely harms many organs, especially the hematopoietic tissue, mandating the development of protective nutraceuticals. MRN-100, a hydro-ferrate fluid, has been shown to protect γ-radiated fish against hematopoietic tissue damage and lethality. The current study aimed to examine MRN-100's protective effect against irradiated mice and explore the mechanisms underlying its effect. Mice received a single acute, sub-lethal, 5 Gy, whole body dose of X-ray IR. MRN-100 treatment was administered daily for 2-weeks pre-irradiation until 1-week post-irradiation. Spleen and blood were analysed for oxidative stress, hematological, histological and biochemical parameters. Radiation exposure markedly decreased complete blood count (CBC) parameters including hemoglobin, hematocrit, red blood cells, platelets, white blood cells and lymphocytes, and significantly increased neutrophils. In contrast, MRN-100 supplementation to irradiated mice ameliorated all CBC parameters and protected against DNA damage in both splenic cells and serum. It also had an antioxidant effect, increasing the levels of glutathione, superoxide dismutase, catalase and total antioxidant capacity, which were otherwise decreased by irradiation. MRN-100 intake reduced the oxidative stress biomarker levels of nitric oxide, protein carbonyl, malondialdehyde, reactive oxygen species and 8-hydroxydeoxyguanosine, a marker specific to DNA damage. Furthermore, MRN-100 enhanced serum iron and reversed the radiation-induced elevations of liver enzymes. Finally, MRN-100 protected splenic tissue from irradiation as observed by histology. We conclude that MRN-100 consumption may protect against oxidative stress generated by radiation exposure, suggesting that it may be employed as an adjuvant treatment to prevent radiation's severe damage to important organs.

Effect of postharvest nicotinamide treatment on NAD+ metabolism and redox status in strawberry fruit during storage.

The increased activity of PARP enzymes is associated with a deficiency of NAD+, as well as with a loss of NADPH and ATP, and consequent deterioration of the redox state in fruits. In this study, we checked whether treatment with nicotinamide (NAM) would affect PARP-1 expression and NAD+ metabolism in strawberry fruit during storage. For this purpose, strawberry fruits were treated with 10 mM NAM and co-treated with NAM and UV-C, and then stored for 5 days at 4 °C. Research showed that nicotinamide contributes to reducing oxidative stress level by reducing PARP-1 mRNA gene expression and the protein level resulting in higher NAD+ availability, as well as improving energy metabolism and NADPH levels in fruits, regardless of whether they are exposed to UV-C. The above effects cause fruits treated with nicotinamide to be characterised by higher anti-radical activity, and a lower level of reactive oxygen species in the tissue.

Antioxidative and Mitochondrial Protection in Retinal Pigment Epithelium: New Light Source in Action.

Low-color-temperature light-emitting diodes (LEDs) (called 1900 K LEDs for short) have the potential to become a healthy light source due to their blue-free property. Our previous research demonstrated that these LEDs posed no harm to retinal cells and even protected the ocular surface. Treatment targeting the retinal pigment epithelium (RPE) is a promising direction for age-related macular degeneration (AMD). Nevertheless, no study has evaluated the protective effects of these LEDs on RPE. Therefore, we used the ARPE-19 cell line and zebrafish to explore the protective effects of 1900 K LEDs. Our results showed that the 1900 K LEDs could increase the cell vitality of ARPE-19 cells at different irradiances, with the most pronounced effect at 10 W/m2. Moreover, the protective effect increased with time. Pretreatment with 1900 K LEDs could protect the RPE from death after hydrogen peroxide (H2O2) damage by reducing reactive oxygen species (ROS) generation and mitochondrial damage caused by H2O2. In addition, we preliminarily demonstrated that irradiation with 1900 K LEDs in zebrafish did not cause retinal damage. To sum up, we provide evidence for the protective effects of 1900 K LEDs on the RPE, laying the foundation for future light therapy using these LEDs.

Radioprotective Effect of Nigella Sativa Oil on Heart Tissues of Rats Exposed to Irradition

Abstract Background Various studies are ongoing related to the radioprotective agents. Herbal preparations are currently becoming popular because of their beneficial effects with fewer side effects compared to the synthetic/semi-synthetic medicines, and Nigella sativa oil (NSO) is only one of them. Objective To investigate NSO for its antioxidant effects on the heart tissue of rats exposed to ionizing radiation (IR). Methods Thirty six male albino Wistar rats, divided into four groups, were designated to group I (IR plus NSO group) that received both 5 Gray of gamma IR to total cranium and NSO; group II (IR alone group) that received IR plus saline, group III (control group of NSO) that received saline and did not receive NSO or IR; group IV (control group) that received only sham IR. Alterations in Total antioxidant status (TAS) and Total oxidant status (TOS), Oxidative stres index (OSI), Sulhydryl group (SH), Lipid hydroperoxide (LOOH), Paraoxonase (PON) levels, Arylesterase (ARE) and Ceruloplasmin (CER) activities in homogenized heart tissue of rats were measured by biochemical methods. Results In heart tissue of the rats in the IR alone group (group II) LOOH, TOS and OSI levels were found to be higher, ARE activity and TAS level were found to be lower than all of the other groups (p < 0.01). These results also support that IR increases oxidative stress and NSO's protective effect. Conclusion NSO would reduce the oxidative damage in the irradiated heart tissue in the experimental rat model.

Hydrogen peroxide can be a plausible biomarker in cyanobacterial bloom treatment.

The effect of combined stresses, photoinhibition, and nutrient depletion on the oxidative stress of cyanobacteria was measured in laboratory experiments to develop the biomass prediction model. Phormidium ambiguum was exposed to various photosynthetically active radiation (PAR) intensities and phosphorous (P) concentrations with fixed nitrogen concentrations. The samples were subjected to stress assays by detecting the hydrogen peroxide (H2O2) concentration and antioxidant activities of catalase (CAT) and superoxide dismutase (SOD). H2O2 concentrations decreased to 30 µmol m-2 s-1 of PAR, then increased with higher PAR intensities. Regarding P concentrations, H2O2 concentrations (nmol L-1) generally decreased with increasing P concentrations. SOD and CAT activities were proportionate to the H2O2 protein-1. No H2O2 concentrations detected outside cells indicated the biological production of H2O2, and the accumulated H2O2 concentration inside cells was parameterized with H2O2 concentration protein-1. With over 30 µmol m-2 s-1 of PAR, H2O2 concentration protein-1 had a similar increasing trend with PAR intensity, independently of P concentration. Meanwhile, with increasing P concentration, H2O2 protein-1 decreased in a similar pattern regardless of PAR intensity. Protein content decreased with gradually increasing H2O2 up to 4 nmol H2O2 mg-1 protein, which provides a threshold to restrict the growth of cyanobacteria. With these results, an empirical formula-protein (mg L-1) = - 192*Log((H2O2/protein)/4.1), where H2O2/protein (nmol mg-1) = - 0.312*PAR2/(502 + PAR2)*((25/PAR)4 + 1)*Log(P/133,100), as a function of total phosphorus concentration, P (µg L-1)-was developed to obtain the cyanobacteria biomass.

NMN recruits GSH to enhance GPX4-mediated ferroptosis defense in UV irradiation induced skin injury.

Oxidative stress and lipid peroxidation are major causes of skin injury induced by ultraviolet (UV) irradiation. Ferroptosis is a form of regulated necrosis driven by iron-dependent peroxidation of phospholipids and contributes to kinds of tissue injuries. However, it remains unclear whether the accumulation of lipid peroxides in UV irradiation-induced skin injury could lead to ferroptosis. We generated UV irradiation-induced skin injury mice model to examine the accumulation of the lipid peroxides and iron. Lipid peroxides 4-HNE, the oxidative enzyme COX2, the oxidative DNA damage biomarker 8-OHdG, and the iron level were increased in UV irradiation-induced skin. The accumulation of iron and lipid peroxidation was also observed in UVB-irradiated epidermal keratinocytes without actual ongoing ferroptotic cell death. Ferroptosis was triggered in UV-irradiated keratinocytes stimulated with ferric ammonium citrate (FAC) to mimic the iron overload. Although GPX4 protected UVB-injured keratinocytes against ferroptotic cell death resulted from dysregulation of iron metabolism and the subsequent increase of lipid ROS, keratinocytes enduring constant UVB treatment were markedly sensitized to ferroptosis. Nicotinamide mononucleotide (NMN) which is a direct and potent NAD+ precursor supplement, rescued the imbalanced NAD+/NADH ratio, recruited the production of GSH and promoted resistance to lipid peroxidation in a GPX4-dependent manner. Taken together, our data suggest that NMN recruits GSH to enhance GPX4-mediated ferroptosis defense in UV irradiation-induced skin injury and inhibits oxidative skin damage. NMN or ferroptosis inhibitor might become promising therapeutic approaches for treating oxidative stress-induced skin diseases or disorders.

Effects of Sargassum virgatum extracts on the testicular measurements, genomic DNA and antioxidant enzymes in irradiated rats.

BACKGROUND: Oxidative stress and reactive oxygen species (ROS) are primarily responsible for the development of male infertility after exposure to γ-irradiation. The present work aimed to assess the ameliorative and therapeutic roles of the aqueous and ethanolic extracts of the edible seaweed Sargassum virgatum (S. virgatum) on spermatogenesis and infertility in γ-irradiated Wistar rats. MATERIALS AND METHODS: Induction of infertility was performed by exposing the rats to 137Cs-gamma rays, using a single dose of 3.5 Gy. γ-irradiated rats were given the S. virgatum ethanolic (S. virgatum-EtOH) and aqueous extracts intraperitoneally on a daily base for two consecutive weeks at doses of 100 and 400 mg/kg body weight (b.wt.) for each seaweed extract. Morphometric data of the testes, semen quality indices, antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx), and deoxyribonucleic acid (DNA) fragmentation were assessed. The results obtained were taken during two-time intervals of 15 and 60 days from the commencement of the algal treatments. In vitro antioxidant assays and polyphenolic compounds of S. virgatum were characterized. RESULTS: Significant negative changes in the semen quality and morphometric data of the testes, as well as remarkable DNA fragmentation, were detected in the irradiated rats compared to the control. The levels of the endogenous antioxidant enzymes (SOD, CAT, GSH, and GPx) were also significantly diminished. Nonetheless, treatments of γ-irradiated rats with the S. virgatum-EtOH and aqueous extracts significantly improved the above-mentioned enzymes, in addition to noteworthy amendments in the dimensions of the testes, the semen quality, as well as the DNA structure. CONCLUSIONS: The ameliorative potency of S. virgatum to cure γ-irradiation-induced male infertility, particularly 400 mg/kg ethanolic extract for 60 days, is the result of the consistent therapeutic interventions of its potent antioxidant and anti-apoptotic polyphenols, particularly protocatechuic, p-hydroxybenzoic, rosmarinic, chlorogenic, cinnamic and gentisic acids, as well as the flavonoids catechin, hesperidin, rutin and quercetin. Besides its high-value nutraceutical importance, S. virgatum could be a natural candidate for developing well-accepted radioprotectant products capable of treating γ-irradiation-induced male infertility.

Lotus Seedpod Proanthocyanidins Protect Against Light-Induced Retinal Damage via Antioxidative Stress, Anti-Apoptosis, and Neuroprotective Effects.

BACKGROUND Over-exposure to visible white light can cause retinal damage. Lotus seedpod proanthocyanidins (LSPCs) possess a variety of biological activities, including potent antioxidant and protective effects. Herein, this study observed whether LSPCs can protect against light exposure-induced retinal damage. MATERIAL AND METHODS We randomly separated 40 Prague-Dawley rats into a control group, a light exposure-induced retinal injury model group, and low-dose (50 mg/kg), medium-dose (100 mg/kg), and high-dose (100 mg/kg) LSPCs groups. Light-induced retinal damage models were established by 5000±200 Lx light treatment for 6 h. Five days and 0.5 h before the light treatment, rats in the LSPCs groups were separately administered 50, 100, and 200 mg/kg LSPCs by gavage. After 7 days, H&E staining of retinal sections was performed and the thickness of the ONL was measured. Oxidative stress-related markers and antioxidant enzymes were measured in serum by biochemical testing. TUNEL staining of retinal sections was also performed. Apoptosis-relevant proteins were examined by RT-qPCR and western blotting. GFAP expression was examined with immunohistochemistry. RESULTS Our H&E staining showed that LSPCs can prevent retinal degeneration following light exposure. Histological analysis showed a significant reduction in the ONL thickness of light exposure-induced retinal injury rats, but LSPCs substantially improved the ONL thickness. LSPCs markedly ameliorated the light-induced increase in levels of MDA, NO, and NOS, and decrease in activity of GSH-Px and SOD. Moreover, LSPCs treatment alleviated light-induced retinal apoptosis and limited the light-induced increase in GFAP expression. CONCLUSIONS LSPCs effectively attenuated light-induced retinal damage through antioxidative stress, anti-apoptosis, and neuroprotective effects.

Black tea is more effective than green tea in prevention of radiation-induced oxidative stress in the aorta of rats.

In the work, the effect of black tea on oxidative stress induced in the aorta by irradiation was studied. The efficiency of black and green tea types was compared, and the effect of the main green tea components (-)-epigallocatechin galate (EGCG) and (-)-epigallocatechin (EGC) on the aorta was studied. The activity of ACE in rat aorta segments was determined by measuring the hydrolysis of hippuryl-L-histidyl-L-leucine, and the production of ROS was estimated from the oxidation of dichlorodihydrofluorescein. Black tea prevented the radiation-induced activation of the ACE and suppressed increased ROS production in the aorta of irradiated rats. The IC50 value for the suppression of the irradiation-induced increase in ACE activity is 1 ml of black tea brewed at a rate of 0.17 g/100 ml. Black tea is 12 times more effective than green tea. The administration of both catechin derivatives from green tea to rats leads to an increase in the activity of ACE and the formation of ROS in the aorta. The dose that provided half maximum activation of ACE (EC50) on intraperitoneal (i. p.) injection of galloylated catechins was found to be the same, 0.06-0.07 µg/kg of body weight. Upon intragastric gavage of EGCG, the EC50 value was by one order of magnitude higher, 0.8 µg/kg. Black tea was more effective than green tea in prevention a radiation-induced increase of ACE activity and oxidative stress in the aorta. This difference was explained by a low content of galloylated catechins in black tea.

Photobiomodulation Therapy Attenuates Anxious-Depressive-Like Behavior in the TgF344 Rat Model.

BACKGROUND: Anxious-depressive-like behavior has been recognized as an early endophenotype in Alzheimer's disease (AD). Recent studies support early treatment of anxious-depressive-like behavior as a potential target to alleviate memory loss and reduce the risk of developing dementia. We hypothesize that photobiomodulation (PBM) could be an effective method to alleviate depression and anxiety at the early stage of AD pathogenesis. OBJECTIVE: To analyze the effect of PBM treatment on anxious-depressive-like behavior at the early stage of AD. METHODS: Using a novel transgenic AD rat model, animals were divided into wild-type, AD+sham PBM, and AD+PBM groups. Two-minute daily PBM (irradiance: 25 mW/cm2 and fluence: 3 J/cm2 at the cortical level) was applied transcranially to the brain of AD animals from 2 months of age to 10 months of age. After completing PBM treatment at 10 months of age, behavioral tests were performed to measure learning, memory, and anxious-depressive-like behavior. Neuronal apoptosis, neuronal degeneration, neuronal damage, mitochondrial function, neuroinflammation, and oxidative stress were measured to test the effects of PBM on AD animals. RESULTS: Behavioral tests showed that: 1) no spatial memory deficits were detected in TgF344 rats at 10 months of age; 2) PBM alleviated anxious-depressive-like behavior in TgF344 rats; 3) PBM attenuated neuronal damage, degeneration, and apoptosis; and 4) PBM suppresses neuroinflammation and oxidative stress. CONCLUSION: Our findings support our hypothesis that PBM could be an effective method to alleviate depression and anxiety during the early stage of AD development. The mechanism underlying these beneficial effects may be due to the improvement of mitochondria function and integrity and the inhibition of neuroinflammation and oxidative stress.

Protective Effects of Ocimum gratissimumAqueous Extracts on HaCaT Cells Against UVC-Induced Inhibition of Cell Viability and Migration.

Ultraviolet C (UVC) has been applied to treatment of infections in wounds for at least the last two decades, however, cells being treated can be damaged if exposure is prolonged, which calls for protective measures, such as drug or herbal pre-treatment, to minimize damage. Ocimum gratissimum contains plant polyphenols such as isoflavones and caffeic acid, which have antioxidant effects. We hypothesize that Ocimum gratissimum aqueous extracts (OGE) can inhibit UVC-induced oxidative damage on skin cells. In this study, HaCaT skin cells are used to test the protective effects of OGE on cell proliferation and migration after exposure to UVC radiation. Pretreatment with OGE (50~150µg/mL) before 40 J/m2 UVC exposure was able to restore survival from 32.25% to between 46.77% and 68.00%, and 80 J/m2 UVC exposure from 11.49% to between 19.07% and 43.04%. Morphological observation of primarily apoptotic cell death confirms the above findings. The flow cytometry analysis revealed that UVC increased the number of cells at the sub-G1 phase in a dose dependent manner, and when pre-treated with OGE the changes were partially reversed. Moreover, the wound healing test for observing migration showed that UVC 40-80 J/m2 decreased cell migration to 47-28% activity and 100 µg/mL OGE was able to restore cell activity to81-69% at day 3. Based on the above results, we suggest that OGE has a protective effect on UVC-induced inhibition of cell proliferation and migration of skin cells and thus has potential application in wound care.

Thymoquinone, extract from Nigella sativa seeds, protects human skin keratinocytes against UVA-irradiated oxidative stress, inflammation and mitochondrial dysfunction.

Ultraviolet A (UVA) irradiation caused skin keratinocytes to accumulate reactive oxygen species (ROS) leading to the skin injury. Thymoquinone (TQ) was identified as the prominent bioactive ingredient in Nigella sativa seeds which was applied in therapying various human diseases. This study aimed to illustrate the role and mechanism of TQ in UVA-induced skin injury. We pre-treated HaCaT cells with TQ and irradiated them by UVA. MTT and Elisa assays were used to evaluate cell viability and apoptosis, as well as cytokine levels. To detect the related parameters of oxidative stress and mitochondrial function, colorimetry, spectrophotometry, bioluminescence, and dual-luciferase reporter methods were used. RT-qPCR and western blotting were performed for expressions of related mRNAs and proteins. TQ significantly improved the UVA-induced cytotoxicity on HaCaT cells. TQ treatment alleviated the oxidative stress and inflammation in UVA-irradiated keratinocytes. Besides, UVA irradiation promoted mitochondrial dysregulation in HaCaT cells leading to cell apoptosis, which could be reversed by TQ treatment. More importantly, NrF2/ARE pathway was activated in TQ-treated cells, while COX-2 was depressed, and inhibiting the pathway or activating COX-2 blocked the therapeutic effect of TQ on UVA-induced skin cell injury. Our study suggested that TQ treatment attenuated the UVA-induced oxidative and inflammatory responses, as well as mitochondrial apoptosis in keratinocytes by COX-2 inhibition via activating NrF2/ARE pathway. This might be a novel sight for preventing the solar radiation damage to the skin.

Perilla frutescens Extracts Enhance DNA Repair Response in UVB Damaged HaCaT Cells.

Physiological processes in skin are associated with exposure to UV light and are essential for skin maintenance and regeneration. Here, we investigated whether the leaf and callus extracts of Perilla frutescens (Perilla), a well-known Asian herb, affect DNA damage response and repair in skin and keratinocytes exposed to Untraviolet B (UVB) light. First, we examined the protective effects of Perilla leaf extracts in UVB damaged mouse skin in vivo. Second, we cultured calluses using plant tissue culture technology, from Perilla leaf explant and then examined the effects of the leaf and callus extracts of Perilla on UVB exposed keratinocytes. HaCaT cells treated with leaf and callus Perilla extracts exhibited antioxidant activities, smaller DNA fragment tails, and enhanced colony formation after UVB exposure. Interestingly, keratinocytes treated with the leaf and callus extracts of Perilla showed G1/S cell cycle arrest, reduced protein levels of cyclin D1, Cyclin Dependent Kinase 6 (CDK6), and γH2AX, and enhanced levels of phosphorylated checkpoint kinase 1 (pCHK1) following UVB exposure. These observations suggest that the leaf and callus extracts of Perilla are candidate nutraceuticals for the prevention of keratinocyte aging.

Intense Pulsed Light Attenuates UV-Induced Hyperimmune Response and Pigmentation in Human Skin Cells.

The skin of an organism is affected by various environmental factors and fights against aging stress via mechanical and biochemical responses. Photoaging induced by ultraviolet B (UVB) irradiation is common and is the most vital factor in the senescence phenotype of skin, and so, suppression of UVB stress-induced damage is critical. To lessen the UVB-induced hyperimmune response and hyperpigmentation, we investigated the ameliorative effects of intense pulsed light (IPL) treatment on the photoaged phenotype of skin cells. Normal human epidermal keratinocytes and human epidermal melanocytes were exposed to 20 mJ/cm2 of UVB. After UVB irradiation, the cells were treated with green (525-530 nm) and yellow (585-592 nm) IPL at various time points prior to the harvest step. Subsequently, various signs of excessive immune response, including expression of proinflammatory and melanogenic genes and proteins, cellular oxidative stress level, and antioxidative enzyme activity, were examined. We found that IPL treatment reduced excessive cutaneous immune reactions by suppressing UVB-induced proinflammatory cytokine expression. IPL treatment prevented hyperpigmentation, and combined treatment with green and yellow IPL synergistically attenuated both processes. IPL treatment may exert protective effects against UVB injury in skin cells by attenuating inflammatory cytokine and melanogenic gene overexpression, possibly by reducing intracellular oxidative stress. IPL treatment also preserves antioxidative enzyme activity under UVB irradiation. This study suggests that IPL treatment is a useful strategy against photoaging, and provides evidence supporting clinical approaches with non-invasive light therapy.

Effects of Nigella sativa oil and thymoquinone on radiation-induced oxidative stress in kidney tissue of rats.

Ionizing radiation leads to release of free radicals into the systemic circulation from irradiated tissues. These free radicals cause oxidative stress in distant organs. Oxidative status may be reversed by naturally occurring antioxidant agents. The aim of this study was to investigate protective and antioxidant effects of Nigella sativa oil (NSO) and thymoquinone (TQ) in kidney tissue of rats exposed to cranial irradiation. Forty-eight Sprague-Dawley rats were divided into six groups: IR group received irradiation (IR) to total cranium plus saline; IR plus NSO group received IR and NSO; IR plus TQ group received IR and TQ; sham group did not receive NSO, TQ or IR; control group of TQ received dimethyl sulfoxide; control group of NSO received saline. Total oxidant status (TOS), oxidative stress index (OSI) and lipid hydroperoxide (LOOH) levels were studied as oxidative parameters, and total antioxidant status (TAS), total sulfhydryl levels, paraoxonase (PON), ceruloplasmin (Cp) and arylesterase activities were determined as antioxidative parameters in the kidney tissue of rats. Kidney TOS, OSI and LOOH levels were significantly lower in IR plus TQ, IR plus NSO and sham groups compared to IR group (p < 0.001). TAS, PON and Cp activities in IR group were significantly lower compared to the control group (p < 0.001). PON and Cp activities were significantly higher in IR plus NSO and IR plus TQ groups compared to IR group (p < 0.001). In conclusion, free radicals generated by cranial ionizing radiation exposure cause oxidative stress in kidney. NSO and TQ exhibit protective and antioxidant effects against oxidative damage in rats.

Photobiomodulation and Oxidative Stress: 980 nm Diode Laser Light Regulates Mitochondrial Activity and Reactive Oxygen Species Production.

Photobiomodulation with 808 nm laser light electively stimulates Complexes III and IV of the mitochondrial respiratory chain, while Complexes I and II are not affected. At the wavelength of 1064 nm, Complexes I, III, and IV are excited, while Complex II and some mitochondrial matrix enzymes seem to be not receptive to photons at that wavelength. Complex IV was also activated by 633 nm. The mechanism of action of wavelengths in the range 900-1000 nm on mitochondria is less understood or not described. Oxidative stress from reactive oxygen species (ROS) generated by mitochondrial activity is an inescapable consequence of aerobic metabolism. The antioxidant enzyme system for ROS scavenging can keep them under control. However, alterations in mitochondrial activity can cause an increment of ROS production. ROS and ATP can play a role in cell death, cell proliferation, and cell cycle arrest. In our work, bovine liver isolated mitochondria were irradiated for 60 sec, in continuous wave mode with 980 nm and powers from 0.1 to 1.4 W (0.1 W increment at every step) to generate energies from 6 to 84 J, fluences from 7.7 to 107.7 J/cm2, power densities from 0.13 to 1.79 W/cm2, and spot size 0.78 cm2. The control was equal to 0 W. The activity of the mitochondria's complexes, Krebs cycle enzymes, ATP production, oxygen consumption, generation of ROS, and oxidative stress were detected. Lower powers (0.1-0.2 W) showed an inhibitory effect; those that were intermediate (0.3-0.7 W) did not display an effect, and the higher powers (0.8-1.1 W) induced an increment of ATP synthesis. Increasing the power (1.2-1.4 W) recovered the ATP production to the control level. The interaction occurred on Complexes III and IV, as well as ATP production and oxygen consumption. Results showed that 0.1 W uncoupled the respiratory chain and induced higher oxidative stress and drastic inhibition of ATP production. Conversely, 0.8 W kept mitochondria coupled and induced an increase of ATP production by increments of Complex III and IV activities. An augmentation of oxidative stress was also observed, probably as a consequence of the increased oxygen consumption and mitochondrial isolation experimental conditions. No effect was observed using 0.5 W, and no effect was observed on the enzymes of the Krebs cycle.

Curcumin decreases dibutyl phthalate-induced renal dysfunction in Kunming mice via inhibiting oxidative stress and apoptosis.

Curcumin (Cur) has been used extensively in dietary supplement with antioxidant and anti-apoptotic properties. Although dibutyl phthalate (DBP) has adverse effects on the kidney, any association between DBP exposure and the role of Cur is unclear. We tested the hypothesis that exposure to DBP has adverse consequences on renal dysfunction in mice and the potential protective role of Cur in decreasing DBP-induced renal dysfunction via inhibiting oxidative stress and apoptosis. Kidney function, oxidative stress biomarkers, and apoptosis factors as well as Bcl-2 and Bax were investigated. The results showed a marked increase of renal dysfunction, oxidative stress and apoptosis level after DBP exposure compared to the control. While administration of Cur to DBP-treated mice may reduce these adverse biochemical changes compared with DBP-alone group. Overall, these results suggest that oxidative stress and apoptosis are involved in DBP-induced renal disorder, whereas Cur plays a protective role in inhibiting these two pathways.

Obacunone protects retinal pigment epithelium cells from ultra-violet radiation-induced oxidative injury.

Ultra-violet (UV) radiation (UVR) causes significant oxidative injury to retinal pigment epithelium (RPE) cells. Obacunone is a highly oxygenated triterpenoid limonoid compound with various pharmacological properties. Its potential effect in RPE cells has not been studied thus far. Here in ARPE-19 cells and primary murine RPE cells, obacunone potently inhibited UVR-induced reactive oxygen species accumulation, mitochondrial depolarization, lipid peroxidation and single strand DNA accumulation. UVR-induced RPE cell death and apoptosis were largely alleviated by obacunone. Obacunone activated Nrf2 signaling cascade in RPE cells, causing Keap1-Nrf2 disassociation, Nrf2 protein stabilization and nuclear translocation. It promoted transcription and expression of antioxidant responsive element-dependent genes. Nrf2 silencing or CRISPR/Cas9-induced Nrf2 knockout almost reversed obacunone-induced RPE cytoprotection against UVR. Forced activation of Nrf2 cascade, by Keap1 knockout, similarly protected RPE cells from UVR. Importantly, obacunone failed to offer further RPE cytoprotection against UVR in Keap1-knockout cells. In vivo, intravitreal injection of obacunone largely inhibited light-induced retinal damage. Collectively, obacunone protects RPE cells from UVR-induced oxidative injury through activation of Nrf2 signaling cascade.