Oxidative stress, as mediated by ROS, is a significant factor in initiating the development of age-associated cataracts; D-limonene is a common natural terpene with powerful antioxidative properties which occurs naturally in a wide variety of living organisms. It has been shown to have antioxidant effect; we found that D-limonene can effectively prevent the oxidative damage caused by H2O2 and propose that the main mechanism underlying the inhibitory effects of D-limonene is the inhibition of HLECs apoptosis. In the present study, we used confocal-fluorescence microscopy, flow cytometry analysis, Hoechst staining, H2DCFDA staining, transmission electron microscopy, and immunoblot analysis; the results revealed that slightly higher concentrations of D-limonene (125–1800 μM) reduced the H2O2-induced ROS generation and inhibited the H2O2-induced caspase-3 and caspase-9 activation and decreased the Bcl-2/Bax ratio. Furthermore, it inhibited H2O2-induced p38 MAPK phosphorylation. Thus, we conclude that D-limonene could effectively protect HLECs from H2O2-induced oxidative stress and that its antioxidative effect is significant, thereby increasing the cell survival rate.

Together our data indicate that low BCAA levels inhibit fatty acid synthesis and enhanced fatty acid β-oxidation in the liver of female broiler chickens and these effects were probably mediated through AMPK-mTOR-FoxO1 pathway.

Oxidative stress plays a significant role in pathophysiology of cataracts and also known to affect the phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) signaling pathway. This well-documented pathway is involved in protecting against apoptosis-inducing insults, including oxidative stress. Melatonin (N-acetyl-5-methoxy-tryptamine), the major secretory product of the pineal gland, was identified as a powerful free radical scavenger and a broad-spectrum antioxidant that defends against various oxidative stress-associated diseases. This study was conducted to determine whether melatonin could prevent hydrogen peroxide (H₂O₂)-induced oxidative stress in human lens epithelial cells (HLECs) and to elucidate the molecular pathways involved in this protection. HLECs were subjected to various concentrations of H₂O₂ in the presence or absence of melatonin at different concentrations. Cell viability was monitored by a 3-(4, 5-dimethylthiazol-2yl)-2, 5-diphenyl-tetrazoliumbromide (MTT) assay, and the apoptosis rate and intracellular reactive oxygen species (ROS) levels were measured by flow cytometry using annexin V-FITC and propidium iodide (PI) staining. The expression levels of HO-1, Nrf-2, CAT, and MDA were measured using Western blot analysis. Akt activation was also evaluated by Western blot analysis. The data from our study showed that cells pretreated with melatonin can reduce H₂O₂-induced intracellular ROS generation and thus protect HLECs from cell apoptosis. Furthermore, we found that melatonin is a potent activator of Akt in HLECs. Our findings suggest that in addition to functioning as a direct free radical scavenger, melatonin can elicit cellular signaling pathways that are protective against oxidative stress-induced cataracts.

Oxidative stress has been recognized as an important mediator in the pathogenesis of age-related cataracts; using antioxidant supplements is one plausible strategy to protect the antioxidative defense system against oxidative stress. Ghrelin administration is expected to reduce ROS, preventing the onset of different diseases. The role of ghrelin, if any, in protecting against oxidative stress in HLECs has never been examined. In the present study, we investigated the effects of ghrelin against H2O2-induced oxidative stress and the associated molecular mechanisms in HLECs and rat lenses. The results showed that pretreatment with ghrelin reduced H2O2-induced cellular apoptosis and ROS accumulation, increased the expression levels of SOD and CAT, and decreased the expression level of MDA. The morphological examination showed that the ghrelin-treated lens organ culture maintained transparency. This is the first report to show that ghrelin can protect HLECs from H2O2-induced oxidative stress. Our findings suggest that ghrelin may prevent the progression of cataracts, which has treatment value for ophthalmologists.