M. Luisa García

Effect of combined ultrasonic and heat treatment (thermoultrasonication) on the survival of a strain of Staphylococcus aureus

The combined effect of ultrasonic waves (20 kHz, 150 W) and heat treatment applied simultaneously (thermoultrasonication) on the survival of a strain of Staphylococcus aureus was studied in 0.05 M-phosphate buffer pH 6.8 and ultra-heat-treated whole milk. This combined process decreased by 63% the decimal reduction times for the heat treatment when the organism was suspended in buffer and by 43% when suspended in milk. These effects were much greater than the additive effect of the two agents considered independently.

Beef hamburgers enriched in lycopene using dry tomato peel as an ingredient.

The direct addition of dry tomato peel (DTP) to hamburgers may be useful both to obtain a new product enriched in lycopene and for providing a use for this by-product from the tomato industry. In this study, different amounts of DTP (0-6.0%w/w) were added to raw and cooked hamburgers, and the effects on the meats physico-chemical and sensorial characteristics were studied. The maximum DTP concentration compatible with good sensory acceptability and high lycopene content was determined. Addition of DTP increased the colour parameters a(∗) and b(∗) of raw and cooked hamburgers, and modified all textural properties probably because of the presence of fibre. The hardness values of cooked samples was significantly higher in the batch containing 6% DTP (67.6N) than in a control batch (50.9N, p<0.05). The addition of DTP to 4.5% results in hamburgers with good overall acceptability and a lycopene content of 4.9mg/100g of cooked hamburger.

Structure-based design of cyclooxygenase-2 selectivity into ketoprofen.

We have recently described how to achieve COX-2 selectivity from the non-selective inhibitor indomethacin (1) using a combination of a pharmacophore and computer 3-D models based on the known X-ray crystal structures of cyclooxygenases. In the present study we have focused on the design of COX-2 selective analogues of the NSAID ketoprofen (2). The design is similarly based on the combined use of the previous pharmacophore together with traditional medicinal chemistry techniques motivated by the comparative modeling of the 3-D structures of 2 docked into the COX active sites. The analysis includes use of the program GRID to detect isoenzyme differences near the active site region and is aimed at suggesting modifications of the basic benzophenone frame of the lead compound 2. The resulting series of compounds bearing this central framework is exemplified by the potent and selective COX-2 inhibitor 17 (LM-1669).

Cell surface hydrophobicity and attachment of pathogenic and spoilage bacteria to meat surfaces.

Cell surface hydrophobicity of several pathogenic and spoilage bacteria was determined by hydrocarbon adherence, adhesion to nitrocellulose filter, salt aggregation and adherence to phenyl-sepharose beads. Hydrophobicity of each bacterium was dependent on the method of measurement. Hydrophobicity was compared with the strength of attachment (Sr) of the bacteria to beef muscle surfaces. Bacterial cell surface hydrophobicity, as determined by the bacterial adherence to xylene correlated well with attachment strength (r = 0.800, P < 0.05). Staphylococcus aureus, Clostridium perfringens and Yersinia enterocolitica showed the highest values of attachment strength.

Analgesic, Antiinflammatory, and Antipyretic Effects of S(+)‐Ketoprofen In Vivo

Many studies indicate that the S‐enantiomers of arylpropionic (APA) nonsteroidal antiinflammatory drugs (NSAIDs) are the pharmacologically active enantiomers. S(+)‐ketoprofen (dexketoprofen) stereoselectively inhibits cyclooxygenase (COX) in vitro but very little is known about the differential activity of ketoprofen enantiomers in vivo. We examined the analgesic, antiinflammatory, and antipyretic activities of S(+)‐ketoprofen in rats and mice. First, we measured the antinociceptive action of S(+)‐ketoprofen in abdominal pain models. After intravenous administration, 0.5 mg/kg S(+)‐ketoprofen inhibited 92.1 ± 2.2% of writhing in mice. Stereoselectivity in the activity was detected; intravenous administration of the R(−)‐enantiomer resulted in no statistically significant activity in a dose range of 0.15–1 mg/kg. Similar results were obtained after oral administration in mice. In the rat, S(+)‐ketoprofen was a more potent analgesic than diclofenac by both intravenous and oral administration. There was no significant difference between the analgesic effect of S(+)‐ketoprofen treatment and the twofold dose of the racemic form in both the mouse and rat models. Second, we measured the antiinflammatory activity of S(+)‐ketoprofen using a carrageenan‐induced paw edema model in the rat. Intravenous administration of 5 mg/kg of S(+)‐ketoprofen almost completely inhibited edema formation. After oral administration, S(+)‐ketoprofen is both more potent and effective than diclofenac. Third, we measured antipyretic activity. S(+)‐ketoprofen showed a marked antipyretic action (ED50 = 1.6 mg/kg) and was the most potent of the NSAIDs tested. S(+)‐ketoprofen is a potent antiinflammatory, analgesic, and antipyretic agent in vivo, consistent with its potent anti‐COX activity.

Intestinal ulcerogenic effect of S(+)-ketoprofen in the rat

Nonsteroidal antiinflammatory drugs (NSAIDs) inhibit prostaglandin synthesis in the gastrointestinal mucosa, which can lead not only to stomach ulcers but also ulcers in the small and large intestines. Ulcers of the small intestine are less common than those of the stomach, but intestinal lesions are more life threatening. Although the R(−)‐enantiomers of the arylpropionic acid (APA) class of NSAIDs are assumed to lack the toxic effects of cyclooxygenase inhibition, they may contribute to the ulcerogenicity of racemates. We have examined the intestinal ulcerogenic effects of single oral doses of S(+)‐ketoprofen compared with racemic ketoprofen in the small intestine and cecum of rats. The toxicity in the small intestine was measured as the weight ratio between portions of intestine showing lesions and the total weight of the tissue. Toxicity in the cecum was evaluated by measuring the size of the ulcers. S(+)‐ketoprofen had no significant ulcerogenic effect at 10 or 20 mg/kg. However, racemic ketoprofen was clearly ulcerogenic in the small intestine and cecum at the 40 mg dose. R(−)‐ketoprofen at 20 mg/kg does not show any effect in the cecum and only limited ulcerogenesis in the small intestine: The latter effect may be the result of racemic inversion. Therefore, the ulcerogenic action of racemic ketoprofen can be interpreted as a synergism between S(+)‐ and R(−)‐ketoprofen. The mechanism of this synergism is not well understood but may be a general feature of APA NSAIDs.

Effect of E-Beam Treatment on the Chemistry and on the Antioxidant Activity of Lycopene from Dry Tomato Peel and Tomato Powder

Tomato powder (TP) and dry tomato peel (DTP) have been previously used in our laboratory as a source of lycopene to manufacture meat products ready-to-eat (RTE) submitted to E-beam irradiation with good technological and sensory results. Present work describes the studies performed in order to investigate the effect of radiation on chemical changes and antioxidant properties of lycopene. DTP and TP were irradiated (4 kGy). Changes on lycopene were analyzed by HPLC; inhibition of reactive oxygen species (ROS), possible modulation of mitogen-activated protein kinases (MAPK) cascade, nuclear factor κ-light-chain-enhancer of activated B cells (NP-κB) activation and expression of proteins involved in oxidation stress were analyzed in RAT-1 fibroblasts cell culture. Radiation reduced the content of all-E-lycopene and increased (Z)-lycopene, lycopene isomerization, and degradation being higher in DTP than in TP. E-Beam treatment increased the antioxidant ability of both DTP and TP in inhibiting spontaneous and H2O2-induced oxidative stress in cultured fibroblasts. Antioxidant activity was higher in DTP than in TP samples.

Bioavailability of S(+)-ketoprofen after oral administration of different mixtures of ketoprofen enantiomers to dogs.

Recent reports have disagreed on whether the bioavailability of S(+)‐ketoprofen is affected by the presence of R(−)‐ketoprofen. To examine this directly, we designed a randomized crossover study in beagle dogs. [14C]‐ S(+)‐ketoprofen trometamol and R(−)‐ketoprofen trometamol were administered in the following percentage ratios: A, 99:1; B, 95:5; C, 90:10; D, 70:30; E, 50:50. Treatments were administered as a single oral dose of 1 mg/kg trometamol salt. Each of eight dogs received all five combinations in random order with a 1‐week washout period between doses. Blood samples were taken before drug administration and at regular intervals for 240 min after dosing. A progressive increase in the plasma concentration of [14C]‐S(+)‐ketoprofen was observed on going from treatment E (lowest dose of S‐enantiomer) to treatments containing the highest doses of (14C]‐S(+)‐ketoprofen. When the pharmacokinetic calculations were normalized to the dose of (14C]‐S(+)‐ketoprofen, we found no statistically significant differences among the normalized AUC and Cmax values of the five treatments. Therefore, S(+)‐ketoprofen absorption was linear and was not influenced by the presence of R(−)‐ketoprofen. Furthermore, there were no significant differences in tmax values among treatments, indicating that the rate of S(+)‐ketoprofen absorption was also unaffected by the presence of R(−)‐ketoprofen.