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Low-dose daylight exposure induces nitric oxide release and maintains cell viability in vitro.

ABSTRACT: Any potential positive effects conferred via sunlight exposure have to be carefully balanced against carcinogenic effects. Here we provide evidence UK sunlight exposure upregulates the cardio protectant nitric oxide (NO) within in vitro skin cell lines with negligible increases in DNA damage and cell death at 1 SED, when compared against unexposed samples. The whole of the ultraviolet A (UV-A) spectrum appears to be responsible for NO release, with efficiency higher at exposures closer to shorter UV-A wavelengths and decreasing with wavelength increases. These results support further in vivo work, which could be of benefit for demographics such as the elderly (that exhibit a natural decline in NO bioavailability).

SUBMITTER: Hazell G

PROVIDER: S-EPMC10539323 | biostudies-literature | 2023 Sep

REPOSITORIES: biostudies-literature

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Low-dose daylight exposure induces nitric oxide release and maintains cell viability in vitro.

Hazell Gareth G Khazova Marina M O'Mahoney Paul P

Scientific reports 20230928 1

Any potential positive effects conferred via sunlight exposure have to be carefully balanced against carcinogenic effects. Here we provide evidence UK sunlight exposure upregulates the cardio protectant nitric oxide (NO) within in vitro skin cell lines with negligible increases in DNA damage and cell death at 1 SED, when compared against unexposed samples. The whole of the ultraviolet A (UV-A) spectrum appears to be responsible for NO release, with efficiency higher at exposures closer to shorte ...[more]

PMID: 37770588

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Project description:PurposeTo investigate the combined anti-Acanthamoeba effects of nitric oxide (NO) donors and hypochlorite to maximize amoebicidal outcomes while minimizing damage to human corneal epithelial cells (HCECs).MethodsAcanthamoeba castellanii and primary cultured HCECs and keratocytes were treated with sodium hypochlorite (NaOCl), NO donors (sodium nitroprusside [SNP] and sodium nitrite [NaNO2]), or a combination of hypochlorite and NO donors. The viability of A. castellanii, HCECs, and keratocytes was assessed. Minimal inhibitory concentration (MIC) and fractional inhibitory concentration of NaOCl and NO donors were determined. The activation of mammalian targets of rapamycin (mTOR) and ERK and the expression of nitrite reductase and Nrf2 were assessed in HCECs using Western blot analysis. The cysticidal effects of combined NaOCl and NO donors were also evaluated.ResultsA dose-dependent toxicity was observed in A. castellanii, HCECs, and keratocytes when treated with NaOCl and SNP. The range of tested NaNO2 concentrations showed no significant toxicity to HCECs; however, dose-dependent toxicity to A. castellanii was observed. The MIC of NaOCl against HCECs and A. castellanii was 8.0 mg/mL. The MIC of NaNO2 and SNP was 500 mM and 10 mM in both HCECs and A. castellanii, respectively. Weak attenuation of the mTOR and ERK phosphorylation was observed and Nrf2 expression decreased slightly after exposure of HCECs to 2.0 mg/mL NaOCl. For the combination treatment, NaOCl (0.125 mg/mL) was selected based on the safety of HCECs and the toxicity of A. castellanii. A more potent anti-Acanthamoeba effect and HCEC toxicity were observed when NaOCl was combined with SNP rather than NaNO2.ConclusionsCombined NaOCl and NO donors had a stronger anti-Acanthamoeba effect compared to either drug alone.Translational relevanceThis study demonstrates that the combined use of various drugs for the treatment of Acanthamoeba infection can enhance the anti-Acanthamoeba effect while minimizing the toxicity of the individual drug.

Project description:ObjectiveImpaired endothelial cell (EC) autophagy compromises shear stress-induced nitric oxide (NO) generation. We determined the responsible mechanism.Approach and resultsOn autophagy compromise in bovine aortic ECs exposed to shear stress, a decrease in glucose uptake and EC glycolysis attenuated ATP production. We hypothesized that decreased glycolysis-dependent purinergic signaling via P2Y1 (P2Y purinoceptor 1) receptors, secondary to impaired autophagy in ECs, prevents shear-induced phosphorylation of eNOS (endothelial nitric oxide synthase) at its positive regulatory site S1117 (p-eNOSS1177) and NO generation. Maneuvers that restore glucose transport and glycolysis (eg, overexpression of GLUT1 [glucose transporter 1]) or purinergic signaling (eg, addition of exogenous ADP) rescue shear-induced p-eNOSS1177 and NO production in ECs with impaired autophagy. Conversely, inhibiting glucose transport via GLUT1 small interfering RNA, blocking purinergic signaling via ectonucleotidase-mediated ATP/ADP degradation (eg, apyrase), or inhibiting P2Y1 receptors using pharmacological (eg, MRS2179 [2'-deoxy-N6-methyladenosine 3',5'-bisphosphate tetrasodium salt]) or genetic (eg, P2Y1-receptor small interfering RNA) procedures inhibit shear-induced p-eNOSS1177 and NO generation in ECs with intact autophagy. Supporting a central role for PKCδT505 (protein kinase C delta T505) in relaying the autophagy-dependent purinergic-mediated signal to eNOS, we find that (1) shear stress-induced activating phosphorylation of PKCδT505 is negated by inhibiting autophagy, (2) shear-induced p-eNOSS1177 and NO generation are restored in autophagy-impaired ECs via pharmacological (eg, bryostatin) or genetic (eg, constitutively active PKCδ) activation of PKCδT505, and (3) pharmacological (eg, rottlerin) and genetic (eg, PKCδ small interfering RNA) PKCδ inhibition prevents shear-induced p-eNOSS1177 and NO generation in ECs with intact autophagy. Key nodes of dysregulation in this pathway on autophagy compromise were revealed in human arterial ECs.ConclusionsTargeted reactivation of purinergic signaling and PKCδ has strategic potential to restore compromised NO generation in pathologies associated with suppressed EC autophagy.

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Low-dose daylight exposure induces nitric oxide release and maintains cell viability in vitro.

Publications

Low-dose daylight exposure induces nitric oxide release and maintains cell viability in vitro.

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