Arthrobacter sp. Inoculation Improves Cactus Pear Growth, Quality of Fruits, and Nutraceutical Properties of Cladodes.

A study was undertaken to determine the effects of a strain of Arthrobacter sp., a Plant Growth-Promoting Bacteria (PGPB), on plant phenology and qualitative composition of Opuntia ficus-indica (L.) Mill. fruits and cladodes. The strain was inoculated in soil, and its effects on cactus pear plants were detected and compared to nontreated plants. Compared to the latter, the treatment with bacteria promoted an earlier plant sprouting (2 months before the control) and fruitification, ameliorating fruit quality (i.e., improved fresh and dry weight: + 24% and + 26%, respectively, increased total solid content by 30% and polyphenols concentrations by 22%). The quality and quantity of monosaccharides of cladodes were also increased by Arthrobacter sp. with a positive effect on their nutraceutical value. In summer, the mean values of xylose, arabinose, and mannose were significantly higher in treated compared to not treated plants (+ 3.54; + 7.04; + 4.76 mg/kg d.w. respectively). A similar trend was observed in autumn, when the cladodes of inoculated plants had higher contents, i.e., 33% xylose, 65% arabinose, and 40% mannose, respect to the controls. In conclusion, Arthrobacter sp. plays a role in the improvement of nutritional and nutraceutical properties of cactus pear plants due to its capabilities to promote plant growth. Therefore, these results open new perspectives in PGPB application in the agro-farming system as alternative strategy to improve cactus pear growth, yield, and cladodes quality, being the latter the main by-product to be utilized for additional industrial uses.

Hyperbilirubinaemia in heterozygous beta-thalassaemia is related to co-inherited Gilbert's syndrome.

The reasons why heterozygotes for beta-thalassaemia have considerable variation in serum bilirubin levels are unknown. High levels of bilirubin could be related to the co-inherited Gilbert's syndrome, determined either by mutations of the coding region or by variation in the A(TA)nTAA motif of the promoter of the bilirubin UDP-glucuronosyltransferase gene (UGT-1). We sequenced the coding and the promoter region of UGT-1A or characterized the A(TA)nTAA motif of the promoter by denaturing gel electrophoresis of radioactive amplified products. The results were correlated with bilirubin levels in 49 beta-thalassaemia heterozygotes for codon 39 (CAG --> TAG) nonsense mutation. 21 normal individuals and 32 unrelated patients with Gilbert's syndrome served as controls. The coding sequence region of the UGT-1A was normal. Five beta-thalassaemia heterozygotes, who were homozygous for the extra (TA) bases in the A(TA)nTAA element of the promoter of UGT-1A, the configuration present in homozygosity in Gilbert's syndrome, had higher bilirubin levels compared to those with the (TA)6/(TA)7 or (TA)6/(TA)6 configurations. In the group of 32 patients with Gilbert's syndrome, 31 of whom had the (TA)7/(TA)7 configuration, we detected 14 heterozygotes for beta-thalassaemia, a figure much higher than predicted on the basis of the carrier rate. Homozygosity for the (TA)7 motif, the typical promoter configuration of Gilbert's syndrome, is one of the factors determining hyperbilirubinaemia in heterozygous beta-thalassaemia.

A subnecrogenic dose of diethylnitrosamine is able to initiate hepatocarcinogenesis in the rat when coupled with fasting/refeeding.

Caloric restriction causes a generalized decrease in growth rate and has been repeatedly associated with an inhibitory effect on cancer development in several systems. In contrast, exposure to complete fasting followed by refeeding is a metabolic condition associated with increased cell turnover in different organs, including the liver. The present study examines whether such condition is able to sustain the induction of initiated hepatocytes following a subnecrogenic dose of diethylnitrosamine (DENA). Male Fisher-344 rats were fasted for 4 days and 1 day after refeeding they were given a single dose of DENA (20 or 200 mg/kg body wt, i.p.). Negative and positive control groups were fed ad libitum and injected with 20 and 200 mg/kg of DENA, respectively. One week later all animals were subjected to the resistant hepatocyte model for the selection of hepatocyte nodules and they were killed 2 weeks thereafter. Results indicated the presence of gamma-glutamyltransferase (GGT) positive foci and nodules (38 +/- 7/cm2) in rats regularly fed and given 200 mg/kg of DENA, while virtually no focal lesions (< 1/cm2) were found in the group receiving 20 mg/kg of DENA and fed throughout the experiment. However, a significant number of GGT positive foci/nodules (14 +/- 7) also developed in rats exposed to fasting and given 20 mg/kg of DENA 24 h after refeeding. No evidence of hepatocellular necrosis was found in the latter group following DENA administration. No effect of fasting was observed when rats received 200 mg/kg of DENA. It is concluded that fasting/refeeding provides conditions which are able to sustain initiation in rat liver by a subnecrogenic dose of a carcinogen. These findings are in contrast with the commonly reported inhibitory effect of chronic food restriction on various stages of carcinogenesis, including initiation.