The chemopreventive activity of apple against carcinogenesis: antioxidant activity and cell cycle control.

Apples and their derivatives are rich in phytochemicals, including flavonoids (catechins, flavonols, quercetin) and phenolic acids (quercetin glycosides, catechin, epicatechin, procyanidins), vitamins, and fibers, that confer an important antioxidant property. Chemoprevention is defined by the use of natural or synthetic agents to interfere with the progression, reverse, or inhibit carcinogenesis, thereby reducing the risk of developing clinically invasive disease. The aim of this article is to present data generated from the use of apples as a chemopreventive agent in carcinogenesis using in-vivo and in-vitro test systems. Apple and its bioactive compounds can exert chemopreventive properties as a result of antioxidant activity and cell cycle control. However, future focus of research on apple such as identifying the specific phytochemical responsible for the anticarcinogenic effect, timing of consumption, and adequate amount of apples to achieve the best preventive effect using human large randomized-controlled trials is needed. Furthermore, animal studies are also relevant for better understanding the role of this fruit in human health as well as modulation of degenerative diseases such as cancer. Therefore, this area warrants further investigation as a new way of thinking, which would apply not only to apples but also to other fruit used as promising therapeutic agents against human diseases.

Cytogenetic damage induced by mouthrinses formulations in vivo and in vitro.

The aim of the present study was to comparatively evaluate DNA damage and cellular death in cells exposed to various commercially available mouthrinses: Listerine Cepacol, Plax alcohol free, Periogard, and Plax Whitening. A total of 75 volunteers were included in the search distributed into five groups containing 15 people each for in vivo study. Exfoliated buccal mucosa cells were collected immediately before mouthrinse exposure and after 2 weeks. Furthermore, blood samples were obtained from three healthy donors for in vitro study. The micronucleus test was used to evaluate mutagenicity and cytotoxicity in vivo. The single-cell gel (comet) assay was used to determine DNA damage in vitro. After 2 weeks exposure, Periogard showed 1.8% of micronucleated cells with significant statistical differences (p < 0.05) compared to before exposure (0.27%). Plax Whitening presented high tail moment value (4.5) when compared to negative control (0.6). The addition of all mouthrinses to cells incubated with methyl methanesulfonate did not alter the number of strand breaks in the genetic material. Listerine was able to reduce genetic damage induced by hydrogen peroxide because a decrease of tail moment was noticed. The results of the present study suggest that Periogard and Plax Whitening can induce genetic damage, whereas Listerine is an antioxidant agent. Since DNA damage is considered to be prime mechanism during chemical carcinogenesis, these data may be relevant in risk assessment for protecting human health and preventing carcinogenesis.

Low-level laser irradiation, cyclooxygenase-2 (COX-2) expression and necrosis of random skin flaps in rats.

Skin flaps are still a matter of concern among surgeons, as failures can occur leading to flap necrosis. However, low-level laser irradiation has been reported as an effective tool to improve the viability of ischemic flaps, yet its mechanisms of action remain unclear. We investigated the effect of low-level laser irradiation on the viability of random skin flaps in rats and determined COX-2 expression in the flap pedicle. The study animals comprised 24 EPM-1 Wistar rats which were randomly allocated into three equal groups. A cranially based dorsal random skin flap measuring 10 × 4 cm was created in all the animals. In one group, laser irradiation was simulated (sham group), and in the other two groups the animals were irradiated at 12 points with 0.29 J at 20 mW (energy density 10.36 J/cm(2), irradiance 0.71 W/cm(2)), or with 7.3 J at 100 mW (energy density 260.7 J/cm(2), irradiance 3.57 W/cm(2)). These procedures were applied to the cranial half of the flap immediately after surgery and were repeated on days 2 and 5 after surgery. The percentage necrotic area was determined on day 7 after surgery by the paper template method. The immunohistochemical expression of COX-2 in the samples was given scores from 0 to 3. The necrotic area was smaller in group irradiated at 7.3 J compared to sham-treated group and to the group irradiated at 0.29 J (P < 0.05); there was no difference between the sham-treated group and group irradiated at 0.29 J. COX-2 expression was lower in the group irradiated at 7.3 J than in the sham-treated group and the group irradiated at 0.29 J (P < 0.001). Low-level laser therapy was effective in decreasing random skin flap necrosis in rats using a laser energy of 7.30 J per point. Laser irradiation also decreased the expression of COX-2 in the flap pedicle.

Hyperbaric oxygen therapy protects the liver from apoptosis caused by ischemia-reperfusion injury in rats.

PURPOSE: : The present paper aimed to investigate the role of hyperbaric oxygen treatment (HBO) and the apoptosis in rat liver ischemia-reperfusion injury (IRI). METHODS: : Thirty-seven male Wistar rats were subjected to 30 minutes of hepatic ischemia and 30 minutes of reperfusion and randomly distributed into six groups: G-I/R (n = 8), control without HBO; G-HBO/I (n = 8), HBO only during the ischemia period; G-HBO/R (n = 8), HBO only during the reperfusion period; G-HBO-I/R (n = 8), HBO during both the ischemia and reperfusion periods; G-Sh (n = 3), HBO without ischemia or reperfusion as sham group; G-C (n = 2) for control of current apoptosis expression on the normal liver tissue. HBO was carried out using a transparent, cylindrical acrylic chamber with a pressure of 2.0 ATA. Hepatic samples were stained for caspase-3 cleavage. RESULTS: : Apoptotic cells were identified in all groups. In the hepatic specimens of animals HBO-treated during ischemia (GHBO-I), there was a significant decrease (P < 0.001) in the number of cells undergoing apoptosis (1.62 +/- 0.91). The apoptotic index showed no significant difference in the animals HBO-treated during ischemia/reperfusion (5.75 +/- 1.28) compared with the G-I/R (3.5 +/- 0.75), which had no HBO treatment. The apoptosis index (11.25 +/- 1.90) was significantly higher (P < 0.01) in HBO-treated animals during the reperfusion period when compared with any of the other groups. CONCLUSION: : A favorable effect was obtained when hyperbaric oxygen was administered early during ischemia. The hyperbaric oxygen in later periods of reperfusion was associated with a more severe apoptosis index. (c) 2009 Wiley-Liss, Inc. Microsurgery 2009.

Effects of hyperbaric oxygen therapy on the rat intestinal mucosa apoptosis caused by ischemia-reperfusion injury.

To examine the apoptosis expression in the intestinal mucosa in accordance of different periods of hyperbaric oxygen (HBO) treatment, rats were submitted to 60 min of mesenteric artery and vein ischemia and 60 min of reperfusion occlusion. A group (G-IR) was the control and HBO was applied in the ischemia (GHBO-I), reperfusion (GHBO-R), and ischemia and reperfusion time (GHBO-IR). After 60 min of reperfusion, samples of small bowel were prepared for immunohistochemical expression of caspase-3. The expression of caspase-3 was significantly inferior when HBO was administered in the ischemia (0.16 +/- 0.01) in comparison with the control (0.70 +/- 0.08), but HBO in the further reperfusion (0.84 +/- 0.03) or both ischemia and reperfusion time (0.42 +/- 0.05) was significantly worse. There was a connection between HBO, small bowel I/R injury, and mucosa apoptosis. The favorable effect was obtained when HBO was administered early in the ischemia time.

Effect of different periods of hyperbaric oxygen on ischemia-reperfusion injury of rat skeletal muscle.

The effect of hyperbaric oxygen (HBO) on ischemia-reperfusion injury of skeletal muscle, applied during different periods, was studied in 56 male rats. Animals were subjected to 6-h ischemia by a tourniquet over the major femoral trocanter and 4 (A) or 24 (B) h of reperfusion. HBO was carried out during 1 h in an acrylic chamber at a pressure of 2.0 ATA (100% oxygen): in the last 60 min of ischemia (II), after ischemia, during 1-h reperfusion time (III), and during the last hour of ischemia plus 1-h reperfusion (IV). Group I was the control group. After 4- or 24-h reperfusion, samples of the soleus muscle were stained by H&E and analyzed immunohistochemically. No interstitial hemorrhage, neutrophil infiltrate, or cellular necrosis were induced by HBO. The apoptosis index did not differ among the groups. HBO reduced morphologic alterations and promoted better results when administered in the ischemia plus reperfusion period (GIV).