01/11/2009 

            Lembremos que o inositol é um osmolito kosmotropo potente, isto é, ele funciona como forte estruturador da água citoplasmática: aumento das pontes de hidrogênio. Muitas doenças são produzidas por fatores que desestruturam a água citoplasmática, isto é, diminuem as pontes de hidrogênio.
 
As pontes de hidrogênio são necessárias no intracelular para:

1- estabilizar a conformação das hélices do DNA e do RNA o que permite manter a estrutura da molécula e a sua característica especial do enrolar e desenrolar das hélices,
2- manter a estrutura tridimensional das enzimas e das proteínas,
3- estabilizar a estrutura terciária das enzimas e das proteínas,
4- manter a hidratação das proteínas, ácidos nucléicos e macromoléculas,
5- estabilizar, manter e proteger a membrana citoplasmática e mitocondrial,
6- interferir no potencial de membrana citoplasmático (Em) e no potencial de membrana mitocondrial (Delta-psi mt)
7- interferir na homeostasia dos poros da membrana citoplasmática,
8- interferir na velocidade das reações químicas intracelulares
9- participar das reações de hidrólise,
10- veicular informações, etc....
                                                                    José de Felippe Junior

Inositol supplementation in respiratory distress syndrome: relationship between serum concentration, renal excretion, and lung effluent phospholipids

J Pediatr. 1987 Apr;110(4):604-10
Hallman M, Arjomaa P, Hoppu K.
Inositol or placebo was given to 48 small preterm infants with respiratory distress syndrome (mean birth weight 1365 g, gestational age 30.1 weeks) between 48 hours and 10 days of age. The dose of inositol, 40 mg/kg every 6 hours, was at least as high as amounts received in full preterm human milk feedings. Serum inositol concentration increased between days 2 and 3 from a mean of 566 mumol/L to 823 mumol/L in the infants given supplement and fell from 451 mumol/L to 292 mumol/L in the controls. On day 16, serum inositol values remained higher in the infants given supplement than in those given placebo (mean 334 mumol/L vs 146 mumol/L, P = 0.014). The infants who developed bronchopulmonary dysplasia had significantly higher renal inositol clearance, lower inositol intake, and lower serum inositol concentrations. Inositol supplementation increased the saturated phosphatidylcholine/sphingomyelin ratio in tracheal aspirates. According to these results, supplementation with inositol in preterm infants leads to a rise in serum inositol concentration and improvement in the surfactant phospholipids. Inositol deserves further study as a dietary supplement for immature preterm infants who do not receive full human milk feeds.
PMID: 3559811

Inositol supplementation in premature infants with respiratory distress syndrome

 N Engl J Med. 1992 May 7;326(19):1233-9
Hallman M, Bry K, Hoppu K, Lappi M, Pohjavuori M.

Children's Hospital, University of Helsinki, Finland.
BACKGROUND. Inositol influences cellular function and organ maturation. Feeding premature infants inositol-rich breast milk increases their serum inositol concentrations. Whether inositol supplementation benefits infants receiving fluids for parenteral nutrition, which are inositol-free, is not known. METHODS. We carried out a placebo-controlled, randomized, double-blind trial to determine the effects of administering inositol (80 mg per kilogram of body weight per day) during the first five days of life to 221 infants with respiratory distress syndrome who were receiving parenteral nutrition (gestational age, 24 to 32 weeks; birth weight, less than 2000 g). All the infants were treated with mechanical ventilation and some with surfactant as well. The primary end point was survival at 28 days without bronchopulmonary dysplasia. RESULTS. The 114 patients given inositol had significantly lower mean requirements for inspiratory oxygen (P less than 0.01) and mean airway pressure (P less than 0.05) from the 12th through the 144th hour of life than did the 107 infants given placebo. Eighty-one infants given inositol and 51 given placebo survived without bronchopulmonary dysplasia (71 vs. 55 percent; P = 0.005). In the 65 infants given surfactant, however, inositol had no effect on the degree of respiratory failure. Thirteen infants given inositol and 21 given placebo had retinopathy of prematurity (13 vs. 26 percent; P = 0.022); none of the infants given inositol had stage 4 disease, whereas 7 of those given placebo did (0 vs. 9 percent; P = 0.012). Among the infants given placebo, those who had poor outcomes (death, bronchopulmonary dysplasia, or stage 4 retinopathy of prematurity) had lower serum inositol concentrations during days 2 through 7 than those who had good outcomes (P less than 0.01). CONCLUSIONS. The administration of inositol to premature infants with respiratory distress syndrome who are receiving parenteral nutrition during the first week of life is associated with increased survival without bronchopulmonary dysplasia and with a decreased incidence of retinopathy of prematurity.

Respiratory distress syndrome and inositol supplementation in preterm infants.

Arch Dis Child. 1986 Nov;61(11):1076-83.
Hallman M, Järvenpää AL, Pohjavuori M.
We report a randomised double blind trial of myo-inositol (inositol) supplementation for 10 days in 74 preterm infants with a birth weight less than 2000 g (mean gestational age 29.5 weeks and mean birth weight 1266 g). All infants required artificial ventilation for treatment of respiratory distress syndrome. Inositol (120-160 mg/kg/day) was administered by the ingastric or intravenous route. The 37 infants who received inositol supplementation required less mechanical ventilation during days 4-10, had less failures of indomethacin to close ductus arteriosus, and had less deaths or bronchopulmonary dysplasia, or both, than the infants treated with placebo. There were no detectable adverse effects. These preliminary results suggest that inositol is an important nutrient in immature preterm infants.
PMID: 3539028