Effect of postpartum maternal infection on proteins and trace elements in colostrum and early milk

In developing countries, maternal infections during lactation are common. In this study, we evaluated the effect of acute maternal postpartum infection on the composition of colostrum and early milk with special emphasis on milk proteins and trace elements. The study was carried out in two maternity hospitals in Lima, Peru. Subjects were normally nourished women (body mass index (BMI) > 20.0) who intended to exclusively breastfeed their child and who had fever and clinical symptoms of infection within the first 48 h postpartum ( n = 34). Non-ill women of similar characteristics were selected as controls ( n = 23). Blood and milk samples were taken on days 1 and 14 postpartum. An acute phase response was confirmed by significantly increased serum levels of C-reactive protein in infected women. Serum zinc levels increased significantly from day 1 to day 14, but were not affected by infection. Serum copper levels were significantly higher in ill women than in non-ill women on day 1. All participating women were breastfeeding on day 14. Whey protein levels, the whey/casein ratio and total protein levels decreased significantly with time, but were not affected by infection. There were no differences in milk iron or copper levels with time or infection. Milk zinc levels decreased significantly with time, but were not affected by infection. Maternal infection during the early postpartum period does not appear to adversely affect the initiation of lactation or milk protein and trace element contents.     

Induction of apoptosis by the ginsenoside Rh2 by internalization of lipid rafts and caveolae and inactivation of Akt

Background and purpose:

Lipid rafts and caveolae are membrane microdomains with important roles in cell survival signalling involving the Akt pathway. Cholesterol is important for the structure and function of these microdomains. The ginsenoside Rh2 exhibits anti-tumour activity. Because Rh2 is structurally similar to cholesterol, we investigated the possibility that Rh2 exerted its anti-tumour effect by modulating rafts and caveolae.

Experimental approach:

A431 cells (human epidermoid carcinoma cell line) were treated with Rh2 and the effects on cell apoptosis, raft localization and Akt activation measured. We also examined the effects of over-expression of Akt and active-Akt on Rh2-induced cell death.

Key results:

Rh2 induced apoptosis concentration- and time-dependently. Rh2 reduced the levels of rafts and caveolae in the plasma membrane and increased their internalization. Furthermore, Akt activity was decreased and consequently, Akt-dependent phosphorylation of Bad, a pro-survival protein, was decreased whereas the pro-apoptotic proteins, Bim and Bax, were increased upon Rh2 treatment. Unlike microdomain internalization induce by cholesterol depletion, Rh2-mediated internalization of rafts and caveolae was not reversed by cholesterol addition. Also, cholesterol addition did not restore Akt activation or rescue cells from Rh2-induced cell death. Rh2-induced cell death was attenuated in MDA-MB-231 cells over-expressing either wild-type or dominant-active Akt.

Conclusions and implications:

Rh2 induced internalization of rafts and caveolae, leading to Akt inactivation, and ultimately apoptosis. Because elevated levels of membrane rafts and caveolae, and Akt activation have been correlated with cancer development, internalization of these microdomains by Rh2 could potentially be used as an anti-cancer therapy.