Waste expanded polystyrene modified with H2SO4/biodegradable chelating agent for reuse: As a highly efficient adsorbent to remove fluoroquinolone antibiotic from water.

Untreated wastewater containing fluoroquinolone antibiotics poses serious hazards to aquatic species and human health; therefore, treatment of waste expanded polystyrene (EPS) is a crucial environmental matter. In this study, waste EPS was modified with a H2SO4/biodegradable chelating agent, [S,S]-ethylenediamine-N,N'-disuccinic acid (EDDS), and used for highly efficient adsorption of the fluoroquinolone antibiotic ciprofloxacin. When ciprofloxacin of 25 mg/L was used, the H2SO4-modified EPS (EPSH2SO4) adsorbed 60.5% of the ciprofloxacin. During sulfonation, adding a low dose of EDDS markedly improved the adsorption ability of EPSH2SO4+EDDS. The optimal modification conditions were 95% H2SO4, 0.002 M EDDS, 80 °C, and 40 min. The increased adsorbent doses enhanced the adsorption. Approximately 0.2 g/L of EPSH2SO4+EDDS could effectively adsorb 97.8% of the ciprofloxacin (554.3 mg/g) within 30 min. Solution pH0 greatly influenced the adsorption, and the most suitable pH0 was 6. The Langmuir isotherm accurately described the adsorption behaviors of both EPSH2SO4 and EPSH2SO4+EDDS (R2 = 0.997-0.998). The adsorption ability of EPSH2SO4+EDDS (qmax = 1250 mg/g) was 32 times higher than that of EPSH2SO4 (qmax = 38.6 mg/g). A total of 1 M HCl effectively regenerated the exhausted adsorbent. The optimal solid/liquid ratio and time were 0.08 g/20 mL and 60 min, respectively. The regenerated EPSH2SO4+EDDS maintained a high adsorption ability (87.2%) after 10 regeneration cycles. The results thus indicate that the EPSH2SO4+EDDS adsorption-regeneration process is a potential approach to remove ciprofloxacin from water.

Rapid modification of waste expanded polystyrene with H2SO4/trace persulfate in one pot for effective adsorption of fluoroquinolone antibiotic and its regeneration.

Norfloxacin, a fluoroquinolone antibiotic, is widely used to treat microbial infections. However, untreated norfloxacin-containing wastewater poses serious threats to the ecosystem and human health. The treatment of waste expanded polystyrene (EPS) by landfilling or incineration could cause environmental problems. In this research, the feasibility of converting EPS into a valuable adsorbent for norfloxacin was evaluated. Results showed that EPS treated with H2SO4 (EPSH2SO4) effectively adsorbed norfloxacin. The optimal sulfonation conditions were 95% H2SO4 and 100 °C. Addition of 0.001 M of persulfate during sulfonation obviously shortened the sulfonation time to 7.5 min, and the adsorption ability of modified EPS increased with increasing persulfate dose. Under the experimental conditions of 25 mg L-1 norfloxacin, pH0 6.2, and 0.4 g L-1 EPSH2SO4+persulfate (dry weight), 97.2% of norfloxacin could be removed after 30 min of adsorption. The adsorption ability of EPSH2SO4+persulfate decreased with increasing solution pH0, and the optimal pH0 was 6.2. The Langmuir isotherm best described the adsorption behavior of EPSH2SO4+persulfate (qmax = 140.9 mg L-1, b = 1.97 L mg-1, R2 = 0.9992). 1 M HCl effectively regenerated the exhausted EPSH2SO4+persulfate at the optimal solid/solution ratio of 8 g L-1. EPSH2SO4+persulfate maintained excellent adsorption capacity (>80.9%) after eight adsorption-regeneration cycles.

Perfluorooctane sulfonate-induced testicular toxicity and differential testicular expression of estrogen receptor in male mice.

Perfluorooctane sulfonate (PFOS, CAS#1763-23-1) causes male reproductive toxicities, but the underlying mechanisms are still unclear. In this study, 0, 0.5 and 10mg/kg/day PFOS were given by oral gavage to adult mice for 5 weeks. In the 10mg/kg group, serum testosterone levels decreased significantly. Sperm counts declined which might be associated with the decreased proliferation and increased apoptosis of germ cells. In relation to increased apoptosis, bax, cleaved caspase-9 and cleaved caspase-3 levels elevated significantly, indicating that PFOS induced germ cell apoptosis by activating the mitochondrial pathway. In addition, the increase in levels of testicular estrogen receptor (ER) ß was observed in both 0.5 and 10mg/kg group, whereas a decrease in ERα expression was only observed in 10mg/kg group. These results suggested that the alterations in testicular ERs expression, together with decreased proliferation and increased apoptosis of germ cells, might be involved in PFOS-induced testicular toxicity.

DNA-dependent protein kinase catalytic subunit (DNA-PKcs)-SIN1 association mediates ultraviolet B (UVB)-induced Akt Ser-473 phosphorylation and skin cell survival.

BACKGROUND: The exposure of skin keratinocytes to Ultraviolet (UV) irradiation leads to Akt phosphorylation at Ser-473, which is important for the carcinogenic effects of excessive sun exposure. The present study investigated the underlying mechanism of Akt Ser-473 phosphorylation by UVB radiation. RESULTS: We found that DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and mammalian target of rapamycin (mTOR) complex 2 (mTORC2) were both required for UVB-induced Akt Ser-473 phosphorylation in keratinocytes. Inhibition of DNA-PKcs activity via its inhibitor NU7026, a dominant-negative kinase-dead mutation, RNA interference (RNAi) or gene depletion led to the attenuation of UVB-induced Akt Ser-473 phosphorylation. Meanwhile, siRNA silencing or gene depletion of SIN1, a key component of mTORC2, abolished Akt Ser-473 phosphorylation by UVB. Significantly, we discovered that DNA-PKcs was associated with SIN1 in cytosol upon UVB radiation, and this complexation appeared required for Akt Ser-473 phosphorylation. Meanwhile, this DNA-PKcs-SIN1 complexation by UVB was dependent on epidermal growth factor receptor (EGFR) activation, and was disrupted by an EGFR inhibitor (AG1478) or by EGFR depletion. UVB-induced complexation between DNA-PKcs and mTORC2 components was also abolished by NU7026 and DNA-PKcs mutation. Finally, we found that both DNA-PKcs and SIN1 were associated with apoptosis resistance of UVB radiation, and inhibition of them by NU7026 or genetic depletion significantly enhanced UVB-induced cell death and apoptosis. CONCLUSION: Taken together, these results strongly suggest that DNA-PKcs-mTORC2 association is required for UVB-induced Akt Ser-473 phosphorylation and cell survival, and might be important for tumor cell transformation.

Deguelin induces both apoptosis and autophagy in cultured head and neck squamous cell carcinoma cells.

Head and neck squamous cell carcinoma (HNSCC) represents more than 5% of all cancers diagnosed annually in United States and around the world. Despite advances in the management of patients with this disease, the survival has not been significantly improved, and the search for potential alternative therapies is encouraging. Here we demonstrate that deguelin administration causes a significant HNSCC cell death. Deguelin induces both cell apoptosis and autophagy by modulating multiple signaling pathways in cultured HNSCC cells. Deguelin inhibits Akt signaling, and down-regulates survivin and cyclin-dependent kinase 4 (Cdk4) expressions, by disrupting their association with heat shock protein-90 (Hsp-90). Deguelin induces ceramide production through de novo synthase pathway to promote HNSCC cell death. Importantly, increased ceramide level activates AMP-activated protein kinase (AMPK), which then directly phosphorylates Ulk1 and eventually leads to cell autophagy. We found that a low dose of deguelin sensitized HNSCC cells to 5-FU. Finally, using a nude mice Hep-2 xenograft model, we also showed a significant anti-tumor ability of deguelin in vivo. Together, we suggest that deguelin may represent a novel and effective chemo-agent against HNSCC.

Sphingosine kinase-1 inhibition sensitizes curcumin-induced growth inhibition and apoptosis in ovarian cancer cells.

Recent published studies suggest that increasing levels of ceramides enhance the chemo-sensitivity of curcumin. Using in vitro approaches, we analyzed the impact of sphingosine kinase-1 (SphK-1) inhibition on ceramide production, and evaluated SphK1 inhibitor II (SKI-II) as a potential curcumin chemo-sensitizer in ovarian cancer cells. We found that SphK1 is overexpressed in ovarian cancer patients' tumor tissues and in cultured ovarian cancer cell lines. Inhibition of SphK1 by SKI-II or by RNA interference (RNAi) knockdown dramatically enhanced curcumin-induced apoptosis and growth inhibition in ovarian cancer cells. SKI-II facilitated curcumin-induced ceramide production, p38 activation and Akt inhibition. Inhibition of p38 by the pharmacological inhibitor (SB 203580), a dominant-negative expression vector, or by RNAi diminished curcumin and SKI-II co-administration-induced ovarian cancer cell apoptosis. In addition, restoring Akt activation introducing a constitutively active Akt, or inhibiting ceramide production by fumonisin B1 also inhibited the curcumin plus SKI-II co-administration-induced in vitro anti-ovarian cancer effect, suggesting that ceramide accumulation, p38 activation and Akt inhibition are downstream effectors. Our findings suggest that low, well-tolerated doses of SKI-II may offer significant improvement to the clinical curcumin treatment of ovarian cancer.

[Ala499Val (C > T) and Lys939Gln (A > C) polymorphisms of the XPC gene: their correlation with male infertility].

OBJECTIVE: The Ala499Val (C > T) and Lys939Gln (A > C) of the XPC gene are two potentially functional nonsynonymous polymorphisms, which affect the rate of DNA repair and might change XPC production and activity. This study aimed to explore the distribution of these two polymorphisms in the Chinese Han population and their relationship with male infertility. METHODS: We genotyped the two polymorphisms of the XPC gene by the PCR-restriction fragment length polymorphism (PCR-RFLP) method in 318 infertile patients and 228 fertile male controls, detected the frequency of the alleles, and analyzed both the individual and the joint contribution of the two polymorphisms to male infertility. RESULTS: For the Ala499Val (C > T) polymorphism, the frequencies of the CC, CT, and TT genotypes were significantly different in distribution between the patients and the controls (P = 0.020). Males with the TT genotype had a lower risk of male infertility than those with the CC genotype (adjusted OR = 0.49, 95% CI: 0.23-0.88), and even lower than those with both CC and CT genotypes (adjusted OR = 0.39, 95% CI: 0.22-0.71). The Lys939Gln (A > C) polymorphism was not related with male infertility. The combined genotype analysis showed that the individuals with 1-4 risk alleles had a significantly higher risk of male infertility (adjusted OR = 2.75, 95% CI = 1.50-5.04) than those with 0 risk allele. CONCLUSION: The Ala499Val (C > T) polymorphism of the XPC gene is correlated with male infertility and may be a potential genetic risk factor for male infertility in the Chinese Han population.

Fenvalerate inhibits the growth of primary cultured rat preantral ovarian follicles.

Fenvalerate is a widely used synthetic pyrethroid insecticide and is reported to disrupt reproductive function in humans and animals. However, little is known about its influence on follicular development. In this study, rat preantral follicles were primary cultured to investigate the effects of fenvalerate on follicular survival rate, morphological change, steroid hormone levels and steroidogenesis related gene mRNA expression. Follicles were cultured with 0, 1, 5 and 25 micromol/L fenvalerate for 72 h. And then the morphous was assessed by conventional light microscopy, steroid hormones were measured by RIA, and the expressions of steroidogenic acute regulatory protein (StAR) and cytochrome P450 side-chain cleavage enzyme (P450scc) were monitored by real-time quantitative PCR analysis. Results showed that fenvalerate inhibited the augmentation of follicular diameters but did not have detectable effects on follicular survival rates. The level of steroid hormones, such as progesterone, testosterone and estradiol, was inhibited. The inhibition might be due to the decreased expression levels of StAR and P450scc. These results suggested that fenvalerate restrained the follicular growth, and inhibited steroidogenesis by reducing StAR and P450scc gene expression, which might further contribute to the fenvalerate-induced reproductive dysfunction.

Localization of epididymal protease inhibitor in adult rat and its transcription profile in testis during postnatal development.

To investigate the expression pattern of rat Eppin (epididymal protease inhibitor; official symbol Spinlw1), we detected mRNA transcripts and subsequent protein translation of Eppin in several sorts of tissues by RT-PCR and western blotting. Then immunohistochemistry was performed for more detailed observation. The testicular transcription level was monitored by real-time PCR throughout postnatal development. We found that rat Eppin was specifically expressed in the testis and epididymis. The testicular transcription was slight in neonatal (1-day) and infantile stages (5-, 7- and 10-day). It increased sharply thereafter, with maximum expression level (about 38-fold compared with that of 1-day old rat) detected in prepubertal stage (15-day). Then a slightly declined but stable level (about 20-fold compared with that of 1-day old rat) was kept in pubertal-early adult (30-day) and adult (60-day) stages of postnatal maturation. In the adult rat, EPPIN protein was mainly localized in the elongated spermatids and epididymal epithelial cells. Sperm in the epididymal duct were all covered with EPPIN and its level kept constant during incubation under conditions used to achieve capacitation. Its stage-specific expression in the testis suggests that EPPIN may be important during spermatogenesis especially for the spermatid elongation. The abundant production of epididymal EPPIN indicated indirectly that it might play a role in the function of the epididymis.

Association of XRCC1 gene polymorphisms with idiopathic azoospermia in a Chinese population.

AIM: To assess the possible role of genetic polymorphisms in DNA repair gene XRCC1 (X-ray repair cross-complementing group 1) during spermatogenesis by investigating the associations of one promoter polymorphism (T-77C) and two exonic polymorphisms (Arg194Trp and Arg399Gln) in XRCC1 gene with risk of idiopathic azoospermia in a Chinese population. METHODS: The genotype and allele frequencies of three observed polymorphisms were examined by polymerase chain reaction-restriction fragment length polymorphism based on a Chinese population consisting of 171 idiopathic azoospermia subjects and 247 normal-spermatogenesis controls. RESULTS: In our study, all the observed genotype frequencies were in agreement with Hardy-Weinberg equilibrium. The 399A (GA+AA) allele frequency for idiopathic azoospermia subjects and controls was 0.216 and 0.269, respectively. Compared with GG genotype, the AA genotype of Arg399Gln showed a significant association with a decreased risk of idiopathic azoospermia (odds ratio = 0.315; 95% confidence interval = 0.12-0.86). However, no significant differences were found between the cases and controls for T-77C and Arg194Trp polymorphisms. The major haplotypes of XRCC1 gene were TCG, TTG and TCA, whereas no haplotypes appeared to be significantly associated with idiopathic azoospermia based on the cutoff of P < 0.05. CONCLUSION: In a selected Chinese population, AA genotype of Arg399Gln appears to contribute to a decreased risk of idiopathic azoospermia, while we have not any evidence of involvement of XRCC1 T-77C and Arg194Trp polymorphisms in idiopathic azoospermia.