Development of Ginkgo (Ginkgo biloba) Nut Starch Films Containing Cinnamon (Cinnamomum zeylanicum) Leaf Essential Oil.

There have been many studies on the development biodegradable films using starch isolated from various food sources as a substitute for synthetic plastic packaging films. In this study, starch was extracted from ginkgo (Ginkgo biloba) nuts, which were mainly discarded and considered an environment hazard. The prepared starch (GBS) was then used for the preparation of antioxidant films by incorporating various amounts of cinnamon (Cinnamomum zeylanicum) essential oil (CZEO), which provides antioxidant activity. The prepared GBS films with CZEO were characterized by measuring physical, optical, and thermal properties, along with antioxidant activity (ABTS, DPPH, and FRAP) measurements. With the increasing amount of CZEO, the flexibility and antioxidant activities of the GBS films increased proportionally, whereas the tensile strength of the films decreased. The added CZEO also increased the water vapor permeability of the GBS films, and the microstructure of the GBS films was homogeneous overall. Therefore, the obtained results indicate that the developed GBS films containing CZEO are applicable as antioxidant food packaging.

Antibacterial activity of the noni fruit extract against Listeria monocytogenes and its applicability as a natural sanitizer for the washing of fresh-cut produce.

This study was conducted to investigate the antibacterial activity of the noni fruit extract (NFE) against Listeria monocytogenes (ATCC, 19111 and 19115) and assess its applicability for the washing of fresh-cut produce. Based on the results of the disc diffusion test, L. monocytogenes (ATCC, 19111 and 19115) was susceptible to the activity of NFE than other pathogens studied. Additionally, results of the time-kill assay indicated that NFE at a concentration of 0.5-0.7% effectively killed L. monocytogenes within 7 h. Furthermore, analysis of the intracellular components such as nucleic acids and proteins released from the bacterial cells and their SEM imaging revealed that NFE could increase the membrane permeability of cells resulting in their death. Compared to their unwashed samples, washing of romaine lettuce, spinach, and kale with 0.5% NFE gave a reduction of 1.47, 2.28, and 3.38 log CFU/g, respectively against L. monocytogenes (ATCC, 19111 and 19115), which is significantly different to that of NaOCl. A significant correlation was observed between the antibacterial effect induced due to NFE washing with the surface roughness of the fresh-cut produce than its surface hydrophobicity. Moreover, washing with NFE was not found to affect the color of the samples. These results indicated that NFE demonstrates good antibacterial activity against L. monocytogenes and can be used as a natural sanitizer to ensure the microbiological safety of fresh-cut produce.

Combined effect of a positively charged cinnamon leaf oil emulsion and organic acid on the inactivation of Listeria monocytogenes inoculated on fresh-cut Treviso leaves.

This study was performed to examine the inhibitory effect of combined treatments with a positively charged cinnamon leaf oil (P-CL) emulsion and various organic acids against Listeria monocytogenes inoculated on fresh-cut Treviso leaves. Combined treatments with a P-CL emulsion and an organic acid exhibited a higher inhibitory effect than treatment with each alone or NaOCl. The highest inhibitory effect was achieved by combined treatment with the P-CL emulsion and lactic acid (LA), which showed a 2.85-log reduction compared to distilled water washing. In addition, the inhibitory effect of the combined treatment was maintained during 6 days of subsequent storage, and showed a 3.24-3.39-log reduction compared to unwashed samples. Treviso leaves treated with the P-CL emulsion and LA also maintained their sensorial properties, including appearance, odor, hardness, freshness, and overall acceptability, during subsequent storage. Therefore, combined treatment with a P-CL emulsion and LA can be used to effectively ensure the microbial safety and organoleptic quality of fresh-cut Treviso leaves.

Characterization of Ecklonia cava Alginate Films Containing Cinnamon Essential Oils.

In this study, Ecklonia cava alginate (ECA) was used as a base material for biodegradable films. Calcium chloride (CaCl2) was used as a cross-linking agent, and various concentrations (0%, 0.4%, 0.7%, and 1.0%) of cinnamon leaf oil (CLO) or cinnamon bark oil (CBO) were incorporated to prepare active films. The ECA film containing 3% CaCl2 had a tensile strength (TS) of 17.82 MPa and an elongation at break (E) of 10.36%, which were higher than those of the film without CaCl2. As the content of essential oils (EOs) increased, TS decreased and E increased. Addition of CLO or CBO also provided antioxidant and antimicrobial activities to the ECA films. The antioxidant activity of the ECA film with CBO was higher than that of the film containing CLO. In particular, the scavenging activities of the 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis (3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) radicals in the ECA film containing 1% CBO were 50.45% and 99.37%, respectively. In contrast, the antimicrobial activities against Escherichia coli O157:H7, Salmonella Typhimurium, Staphylococcus aureus, and Listeria monocytogenes were superior in the ECA films with CLO. These results suggest that ECA films containing CLO or CBO can be applied as new active packaging materials.

Development of Burdock Root Inulin/Chitosan Blend Films Containing Oregano and Thyme Essential Oils.

In this study, inulin (INU) extracted from burdock root was utilized as a new film base material and combined with chitosan (CHI) to prepare composite films. Oregano and thyme essential oils (OT) were incorporated into the INU-CHI film to confer the films with bioactivities. The physical and optical properties as well as antioxidant and antimicrobial activities of the films were evaluated. INU film alone showed poor physical properties. In contrast, the compatibility of INU and CHI demonstrated by the changes in attenuated total reflectance-Fourier transformation infrared spectrum of the INU-CHI film increased tensile strength and elongation at break of the INU film by 8.2- and 3.9-fold, respectively. In addition, water vapor permeability, water solubility, and moisture content of the films decreased proportionally with increasing OT concentration in the INU-CHI film. Incorporation of OT also increased the opacity of a and b values and decreased the L value of the INU-CHI films. All INU-CHI films containing OT exhibited antioxidant and antimicrobial properties. Particularly, the INU-CHI film with 2.0% OT exhibited the highest 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid), 2,2-diphenyl-1-picrylhydrazyl radical scavenging, and antimicrobial activities against four pathogens. Thus, the INU-CHI film containing OT developed in this study might be utilized as an active packaging material in the food industry.

DNA damage-induced apoptosis suppressor (DDIAS), a novel target of NFATc1, is associated with cisplatin resistance in lung cancer.

In a previous study, we reported that DNA damage induced apoptosis suppressor (DDIAS; hNoxin), a human homolog of mouse Noxin, functions as an anti-apoptotic protein in response to DNA repair. Here we reveal that DDIAS is a target gene of nuclear factor of activated T cells 2 (NFATc1) and is associated with cisplatin resistance in lung cancer cells. In the DDIAS promoter analysis, we found that NFATc1 activated the transcription of DDIAS through binding to NFAT consensus sequences in the DDIAS promoter. In addition, tissue array immunostaining revealed a correlation between DDIAS and NFATc1 expression in human lung tumors. NFATc1 knockdown or treatment with the NFAT inhibitor cyclosporine A induced apoptosis and led to growth inhibition of lung cancer cells, indicating the functional relevance of both the proteins. In contrast, DDIAS overexpression overcame this NFATc1 knockdown-induced growth inhibition, supporting the cancer-specific role of DDIAS as a target gene of NFATc1. NFATc1 or DDIAS inhibition clearly enhanced apoptosis induced by cisplatin in NCI-H1703 and A549 cells. Conversely, DDIAS overexpression rescued NCI-H1703 cells from cisplatin-mediated cell death and caspase-3/7 activation. These results suggest that NFATc1-induced DDIAS expression contributes to cisplatin resistance, and targeting DDIAS or NFATc1 impairs the mechanism regulating cisplatin resistance in lung cancer cells. Taken together, DDIAS is a target of NFATc1 and is associated with cisplatin resistance in lung cancer cells.

Identification of Targets of the HIF-1 Inhibitor IDF-11774 Using Alkyne-Conjugated Photoaffinity Probes.

We developed a hypoxia-inducible factor-1 (HIF-1) inhibitor, IDF-11774, as a clinical candidate for cancer therapy. To understand the mechanism of action of IDF-11774, we attempted to isolate target proteins of IDF-11774 using bioconjugated probes. Multifunctional chemical probes containing sites for click conjugation and photoaffinity labeling were designed and synthesized. After fluorescence and photoaffinity labeling of proteins, two-dimensional electrophoresis (2DE) was performed to isolate specific molecular targets of IDF-11774. Heat shock protein (HSP) 70 was identified as a target protein of IDF-11774. We revealed that IDF-11774 inhibited HSP70 chaperone activity by binding to its allosteric pocket, rather than the ATP-binding site in its nucleotide-binding domain (NBD). Moreover, IDF-11774 reduced the oxygen consumption rate (OCR) and ATP production, thereby increasing intracellular oxygen tension. This result suggests that the inhibition of HSP70 chaperone activity by IDF-11774 suppresses HIF-1α refolding and stimulates HIF-1α degradation. Taken together, these findings indicate that IDF-11774-derived chemical probes successfully identified IDF-11774's target molecule, HSP70, and elucidated the mode of action of IDF-11774 in inhibiting HSP70 chaperone activity and stimulating HIF-1α degradation in cancer cells.

Application of a puffer fish skin gelatin film containing Moringa oleifera Lam. leaf extract to the packaging of Gouda cheese.

This study aims to develop a puffer fish skin gelatin (PSG) film that contains Moringa oleifera Lam. leaf extract (ME) as a new biodegradable film. With the increase in ME concentration, the tensile strength and elongation at break of the PSG film increased, whereas the oxygen permeability and water vapor permeability decreased. In addition, the PSG film with ME exhibited antimicrobial activity against Listeria monocytogenes and antioxidant activity. To apply the ME-containing PSG film to food packaging, Gouda cheese was wrapped with the ME-containing PSG film. During storage, the cheese packaging with the ME-containing PSG film effectively inhibited the microbial growth and retarded the lipid oxidation of cheese compared with the control sample. Thus, the ME-containing PSG film can be used as an antimicrobial and antioxidative packaging material to improve the quality of food products.

Preparation of a porcine plasma protein composite film and its application.

To use blood released from slaughtering houses, a porcine plasma protein (PPP)/nanoclay composite film was prepared. The tensile strength and elongation at break values of the PPP composite film with 5% nanoclay were 10.01 MPa and 6.55%, respectively. The PPP composite film containing 1% grapefruit seed extract (GSE) was applied to pork meat, and the populations of inoculated Escherichia coli O157:H7 and Listeria monocytogenes in the pork meat packaged with the PPP composite film decreased by 0.8 and 1.0 log CFU/g, respectively, after 7 days of storage compared to the populations of the control. In addition, thiobarbituric acid values in the pork meat packaged with the PPP composite film were less than those of the control sample during storage. These results suggest that the PPP nanocomposite film containing 1% GSE can be used as a packaging material to maintain the quality of pork meat.

Human Noxin is an anti-apoptotic protein in response to DNA damage of A549 non-small cell lung carcinoma.

Human Noxin (hNoxin, C11Orf82), a homolog of mouse noxin, is highly expressed in colorectal and lung cancer tissues. hNoxin contains a DNA-binding C-domain in RPA1, which mediates DNA metabolic processes, such as DNA replication and DNA repair. Expression of hNoxin is associated with S phase in cancer cells and in normal cells. Expression of hNoxin was induced by ultraviolet (UV) irradiation. Knockdown of hNoxin caused growth inhibition of colorectal and lung cancer cells. The comet assay and western blot analysis revealed that hNoxin knockdown induced apoptosis through activation of p38 mitogen-activated protein kinase (MAPK)/p53 in non-small cell lung carcinoma A549 cells. Furthermore, simultaneous hNoxin knockdown and treatment with DNA-damaging agents, such as camptothecin (CPT) and UV irradiation, enhanced apoptosis, whereas Trichostatin A (TSA) did not. However, transient overexpression of hNoxin rescued cells from DNA damage-induced apoptosis but did not block apoptosis in the absence of DNA damage. These results suggest that hNoxin may be associated with inhibition of apoptosis in response to DNA damage. An adenovirus expressing a short hairpin RNA against hNoxin transcripts significantly suppressed the growth of A549 tumor xenografts, indicating that hNoxin knockdown has in vivo anti-tumor efficacy. Thus, hNoxin is a DNA damage-induced anti-apoptotic protein and potential therapeutic target in cancer.

NSC126188 induces apoptosis of prostate cancer PC-3 cells through inhibition of Akt membrane translocation, FoxO3a activation, and RhoB transcription.

We previously reported that NSC126188 caused apoptosis of cancer cells by inducing expression of RhoB. We here present that NSC126188 induces apoptosis of prostate cancer PC-3 cells by inhibiting Akt/FoxO3 signaling, which mediates RhoB upregulation. The apoptosis and Akt dephosphorylation caused by NSC126188 was not substantially relieved by overexpressing wild-type Akt but was relieved by overexpressing constitutively active Akt (CA-Akt) or myristoylated Akt (myr-Akt). Furthermore, overexpression of CA-Akt or myr-Akt downregulated RhoB expression, indicating that RhoB expression is regulated by Akt signaling. Interestingly, membrane translocation of GFP-Akt by insulin exposure was abolished in the cells pretreated with NSC126188 suggesting that NSC126188 directly interfered with translocation of Akt to the plasma membrane. In addition, NSC126188 activated FoxO3a by dephosphorylating S253 via Akt inhibition. Activated FoxO3a translocated to the nucleus and increased transcription of RhoB and other target genes. PC-3 cells transiently overexpressing FoxO3a exhibited increased RhoB expression and apoptosis in response to NSC126188. Conversely, FoxO3a knockdown reduced NSC126188-induced RhoB expression and cell death. These results suggest that RhoB may be a target gene of FoxO3a and is regulated by Akt signaling. Taken together, NSC126188 induces apoptosis of PC-3 cells by interfering with membrane recruitment of Akt, resulting in Akt dephosphorylation and FoxO3a activation, which leads to transcription of RhoB.

Reactive oxygen species-mediated activation of the Akt/ASK1/p38 signaling cascade and p21(Cip1) downregulation are required for shikonin-induced apoptosis.

Shikonin derivatives exert powerful cytotoxic effects, induce apoptosis and escape multidrug resistance in cancer. However, the diverse mechanisms underlying their anticancer activities are not completely understood. Here, we demonstrated that shikonin-induced apoptosis is caused by reactive oxygen species (ROS)-mediated activation of Akt/ASK1/p38 mitogen-activated protein kinase (MAPK) and downregulation of p21(Cip1). In the presence of shikonin, inactivation of Akt caused apoptosis signal-regulating kinase 1 (ASK1) dephosphorylation at Ser83, which is associated with ASK1 activation. Shikonin-induced apoptosis was enhanced by inhibition of Akt, whereas overexpression of constitutively active Akt prevented apoptosis through modulating ASK1 phosphorylation. Silencing ASK1 and MKK3/6 by siRNA reduced the activation of MAPK kinases (MKK) 3/6 and p38 MAPK, and apoptosis, respectively. Antioxidant N-acetyl cysteine attenuated ASK1 dephosphorylation and p38 MAPK activation, indicating that shikonin-induced ROS is involved in the activation of Akt/ASK1/p38 pathway. Expression of p21(Cip1) was significantly induced in early response, but gradually decreased by prolonged exposure to shikonin. Overexpression of p21(Cip1) have kept cells longer in G1 phase and attenuated shikonin-induced apoptosis. Depletion of p21(Cip1) facilitated shikonin-induced apoptosis, implying that p21(Cip1) delayed shikonin-induced apoptosis via G1 arrest. Immunohistochemistry and in vitro binding assays showed transiently altered localization of p21(Cip1) to the cytoplasm by shikonin, which was blocked by Akt inhibition. The cytoplasmic p21(Cip1) actually binds to and inhibits the activity of ASK1, regulating the cell cycle progression at G1. These findings suggest that shikonin-induced ROS activated ASK1 by decreasing Ser83 phosphorylation and by dissociation of the negative regulator p21(Cip1), leading to p38 MAPK activation, and finally, promoting apoptosis.

Development of episomal vectors carrying a nourseothricin-resistance marker for use in minimal media for Schizosaccharomyces pombe.

In the post-genomic era, an immediate challenge is to assign biological functions to novel proteins encoded by the genome. This challenge requires the use of a simple organism as a genetic tool and a range of new high-throughput techniques. Schizosacchromyces pombe is a powerful model organism used to investigate disease-related genes and provides useful tools for the functional analysis of heterologous genes. To expand the current array of experimental tools, we constructed two series of Sz. pombe expression vectors, i.e. general and Gateway vectors, containing nourseothricin-resistance markers. Vectors carrying nourseothricin-resistance markers possess advantages in that they do not limit the parental strains with auxotrophic mutations with respect to availability for use in clone selection and can be used together with vectors carrying nutrient markers in minimal media. We modified the pSLF173, pSLF273 and pSLF373 vectors carrying a triple haemagglutinin epitope (3×HA) and an Ura4 marker. The vectors described here contain the nmt1 promoter with three different episomal expression strengths for proteins fused with 3×HA, EGFP or DsRed at the N-terminus. These vectors represent an important contribution to the genome-wide investigation of multiple heterologous genes and for functional and genetic analysis of novel human genes.

Upregulation of RhoB via c-Jun N-terminal kinase signaling induces apoptosis of the human gastric carcinoma NUGC-3 cells treated with NSC12618.

RhoB expression is reduced in most invasive tumors, with loss of RhoB expression correlating significantly with tumor stage. Here, we demonstrate that upregulation of RhoB by the potent anticancer agent NSC126188 induces apoptosis of NUGC-3 human gastric carcinoma cells. The crucial role of RhoB in NSC126188-induced apoptosis is indicated by the rescue of NUGC-3 cells from apoptosis by knockdown of RhoB. In the presence of NSC126188, c-Jun N-terminal kinase (JNK) signaling was activated, and the JNK inhibitor SP600125 reduced RhoB expression and suppressed the apoptosis of NUGC-3 cells. Knockdowns of mitogen-activated protein kinase kinase (MKK) 4/7, JNK1/2 and c-Jun downregulated RhoB expression and rescued cells from apoptotic death in the presence of NSC126188. The JNK inhibitor SP600125 suppressed transcriptional activation of RhoB in the presence of NSC126188, as indicated by a reporter assay that used luciferase under the RhoB promoter. The ability of NSC126188 to increase luciferase activity through both the p300-binding site and the inverted CCAAT sequence (iCCAAT box) suggests that JNK signaling to upregulate RhoB expression is mediated through both the p300-binding site and the iCCAAT box. However, the JNK inhibitor SP600125 did not inhibit the upregulation of RhoB by farnesyltransferase inhibitor (FTI)-277. The p300-binding site did not affect activation of the RhoB promoter by FTI-277 in NUGC-3 cells, suggesting that the transcriptional activation of RhoB by NSC126188 occurs by a different mechanism than that reported for FTIs. Our data indicate that NSC126188 increases RhoB expression via JNK-mediated signaling through a p300-binding site and iCCAAT box resulting in apoptosis of NUGC-3 cells.

NSC126188, a piperazine alkyl derivative, induces apoptosis via upregulation of RhoB in HeLa cells.

We describe here a piperazine alkyl derivative, NSC126188, which induced apoptosis of HeLa cells by upregulating RhoB expression. NSC126188 caused multi-septation of fission yeast and hypersensitized a ∆rho3 mutant, which implicates the involvement of functional human homolog RhoB. The treatment of cells with NSC126188 induced apoptosis and a dramatic increase in RhoB expression. In addition, RhoB knockdown using siRNA rescued cells from apoptosis, indicating a crucial role of RhoB in NSC126188-induced apoptosis. In a reporter assay using luciferase and EGFP under control of the RhoB promoter, NSC126188 increased both luciferase activity and the expression of EGFP, implicating transcriptional activation of RhoB by NSC126188. Furthermore, NSC126188 demonstrated in vivo anti-tumor activity, inhibiting tumor growth by 66.8% in a nude mouse xenograft using PC-3 human prostate cancer cells. These results suggest that NSC126188 is a potential lead compound and that upregulation of RhoB is associated with NSC126188-induced apoptosis.

Increase of RhoB in gamma-radiation-induced apoptosis is regulated by c-Jun N-terminal kinase in Jurkat T cells.

The Ras-related small GTP-binding protein RhoB is known to be a pro-apoptotic protein and immediate-early inducible by genotoxic stresses. In addition, JNK activation is known to function in gamma-radiation-induced apoptosis. However, it is unclear how JNK activation and gamma-radiation-dependent RhoB induction are related. Here we verified the relationship between JNK activation and RhoB induction. RhoB induction by gamma-radiation occurred at the transcriptional level and transcriptional activation of RhoB was concomitant with an increase in RhoB protein. gamma-Radiation-induced RhoB expression was markedly attenuated by pretreatment with a JNK-specific inhibitor, SP600125, but not by a p38 MAPK inhibitor, SB203580. Inhibition of JNK caused a decrease in early apoptotic cell death that correlated with RhoB expression. However, PI3K inhibition had no significant effects, indicating that the AKT survival pathway was not involved. The siRNA knockdown of JNK resulted in a decrease in RhoB expression and the siRNA knockdown of RhoB restored cell growth even in the gamma-irradiated cells. These results suggest that RhoB regulation involves the JNK pathway and contributes to the early apoptotic response of Jurkat T cells to gamma-radiation.

In vitro degradation of zearalenone by Bacillus subtilis.

Zearalenone (ZEN) is a non-steroidal estrogen produced by many Fusarium species in cereals and other plants, and is frequently implicated in safety of foods and feeds. A ZEN-degrading microorganism has been isolated and identified as a Bacillus subtilis subspecies. It degraded 99% ZEN (1 mg kg(-1)) in liquid medium after 24 h and more than 95% of ZEN (0.25 mg kg(-1)) could be degraded after 48 h in a solid-state fermentation. This isolate can thus be used to decontaminate raw materials, like grains, to reduce the mycotoxin concentration.

Effect of java citronella essential oil addition on the physicochemical properties of Gelidium corneum-chitosan composite films.

A new composite film was developed by combining Gelidium corneum (GC) with chitosan to enhance the physicochemical characteristics of GC film. In addition, to confer new functional property on the GC-chitosan composite film, various amounts (0.5%, 1.0%, and 1.5%) of java citronella essential oil (JCEO) were incorporated into the film. As the concentration of JCEO increased, the extensibility of the GC-chitosan film improved. In addition, the film became more opaque due to decreased light transmission. Especially, ultraviolet light was completely blocked in the composite films containing JCEO. Radical scavenging activities of the films also increased with increasing JCEO content, indicating that the films have antioxidant activity. Therefore, GC-chitosan composite film containing JCEO is applicable in food packaging to preserve food quality by retarding lipid oxidation.

RhoB induces apoptosis via direct interaction with TNFAIP1 in HeLa cells.

RhoB, a tumor suppressor, has emerged as an interesting cancer target, and extensive studies aimed at understanding its role in apoptosis have been performed. In our study, we investigated the involvement of RhoB-interacting molecules in apoptosis. To identify RhoB-interacting proteins, we performed yeast-two hybrid screening assays using RhoB as a bait and isolated TNFAIP1, a TNFalpha-induced protein containing the BTB/POZ domain. The interaction between RhoB and TNFAIP1 was demonstrated in vivo through coimmunoprecipitation studies and in vitro binding assays. RFP-TNFAIP1 was found to be partially colocalized with EGFP-RhoB. The partial colocalization of RhoB and TNFAIP1 in endosomes suggests that RhoB-TNFAIP1 interactions may have a functional role in apoptosis. TNFAIP1 elicited proapoptotic activity, while simultaneous expression of RhoB and TNFAIP1 resulted in a dramatic increase in apoptosis in HeLa cells. Furthermore, knockdown of RhoB using siRNA clearly rescued cells from apoptosis induced by TNFAIP1. This finding suggests that interactions between RhoB and TNFAIP1 are crucial for induction of apoptosis in HeLa cells. The observation of increased SAPK/JNK phosphorylation in apoptotic cells and the finding that a JNK inhibitor suppressed apoptosis indicates that SAPK/JNK signaling may be involved in apoptosis induced by RhoB-TNFAIP1 interactions. In conclusion, we found that RhoB interacts with TNFAIP1 to regulate apoptosis via a SAPK/JNK-mediated signal transduction mechanism.

Disinfection of iceberg lettuce by titanium dioxide-UV photocatalytic reaction.

Securing the physical quality and microbial safety of fresh foods has been a major focus in the food industry. To improve quality and increase the shelf life of fresh produce, disinfection methods have been developed. Titanium dioxide (TiO2) photocatalytic reactions under UV radiation produce hydroxyl radicals that can be used for disinfection of foodborne pathogenic bacteria. We investigated the effects of TiO2-UV photocatalytic disinfection on the shelf life of iceberg lettuce. Counts of natural microflora (total aerobic bacteria, coliforms, psychrotrophic bacteria, and yeasts and molds) and inoculated pathogenic bacteria (Escherichia coli, Listeria monocytogenes, Staphylococcus aureus, and Salmonella Typhimurium) on iceberg lettuce were determined after 20-min treatments with TiO2-UV, UV radiation, a sodium hypochlorite (NaOCl) solution, and tap water. TiO2-UV treatment reduced the number of microorganisms by 1.8 to 2.8 log CFU/g compared with reductions of 0.9 to 1.4 and 0.7 to 1.1 log CFU/g obtained with UV radiation and NaOCl treatments, respectively. Treatment with tap water was used as a control and resulted in no reductions. Counts of microflora for iceberg lettuce at 4 and 25 degrees C were determined during a 9-day period. TiO2-UV treatment resulted in 1.2- and 4.3-log increases in the counts of total aerobic bacteria at 4 and 25 degrees C, respectively, compared with 1.3- to 1.6-log and 4.4- to 4.8-log increases due to UV radiation and NaOCl treatments.