Spermine induced protection of onion seed vigour and viability during accelerated ageing

Aim: The aim of the present study was to investigate the role of spermine, a polyamine as a protective agent on accelerated ageing of onion seeds. Methodology: Onion seeds variety Pusa Riddhi was primed with six concentrations of spermine (0.10 mM to 1.25 mM) and also with hydration and halopriming (2% K2HPO4). Hydrated, haloprimed and un-primed seeds were used as control. The primed and control seeds were accelerated aged at 45 oC and 100 % RH for 72 hr. Seed quality was assessed in control, freshly primed seeds, and in primed seeds subjected to accelerate ageing. Results: All priming treatments enhanced the seed quality, there was 2.34–20.33 % increase in germination. Seed priming with 2% K2HPO4 had highest seed quality improvement which was at par with 1.25 mM spermine primed seeds. Enhanced seed vigour and the activity of antioxidant enzymes over un-primed seeds was observed in both 2% K2HPO4 and spermine primed seeds over unprimed seds. Seeds primed with 1.25 mM spermine recorded 66.66 % and 650 % increase in the activity of ROS scavenging enzymes SOD and POD respectively, but they were at par with halopriming. After accelerated ageing, deterioration in seed quality was minimal in seeds primed with spermine. Seeds primed with 1.25 mM spermine recorded 21.33% higher germination, 62.10 % higher speed of germination, 26.56 % longer seedlings, 13.68 % heavier seedlings and 175 % and 200 % higher SOD and POD activity as comparised to un-primed seeds. Seeds primed with 1.25 mM spermine also performed better over halopriming and hydropriming treatments. Interpretation: Onion seed priming with 1.25 mM spermine was most effective treatment in enhancing the seed germination and vigour under accelerated ageing conditions.

Intestinal infections.

Gastrointestinal infections are the significant cause of childhood morbidity and mortality worldwide. Gastrointestinal infections reflects the balance between the intrinsic virulence factors of the enteropathogens and host mechanisms which defend against enteric infections. Host defense factors include gastric acidity, intestinal motility, the normal indigenous intestinal microflora, mucous secretion, and specific mucosal and systemic immune mechanisms. Majority of GI infections are self limited so on one hand antibiotics are not needed and on the other hand the irrational use of antibiotics produces resistant strains. Acute diarrheal diseases which are one of the important intestinal infections, in majority of the cases are viral and have short course. Antibiotics are recommended only in specific cases and in immunocompromised individuals. Gastrointestinal disease is one of the most common manifestations of HIV infection. The gastrointestinal tract contains abundant quantities of lymphoid tissue and is likely to function as a reservoir of HIV infection, a site of profound immune dysregulation, and a target for opportunistic infections. In this situation specific antibiotics are indicated.

Hepatobiliary abnormalities and parenteral nutrition.

Hepatobiliary dysfunctions (TPN-HBD) occur during parenteral nutrition. In older children these are usually reversible whereas in newborns and infants these hepatobiliary abnormalities play a significant role in the morbidity. Cholestasis is a commonly occurring TPN-HBD. It correlates directly with the decreasing gestational age, low birth weight and increasing duration of TPN therapy. The pathogenesis of cholestasis of TPN is multifactorial and predisposed by necrotising enterocolitis, sepsis, cardiac failure, shock, and hypotension. Diagnosis is made with exclusion of other causes of direct hyperbilirubinemia. Most TPN-HBD appear within 4 weeks of starting of TPN but severe complications manifest usually after the 16th week. Histologically there is intralobular cholestasis. In few cases there may be severe portal fibrosis followed by development of micronodular biliary cirrhosis. Enteral starvation, defective bile acid carriers, hypercaloric TPN are the major factors responsible for TPN-HBD, including cholestasis. Biliary complications of TPN-HBD are acalculous, cholecystitis, and cholelithiasis. Bile stasis is a major pathological factor for these. If the calories are provided only by glucose or glucose-containing electrolyte solutions it may lead to cholestasis and other TPN-HBD. Even small oral alimentation (continuous or bolus) during TPN, prevent TPN-HBD. Choleretic agents have been useful in the prevention and management of cholestasis and other parenteral nutrition induced hepatobiliary abnormalities.