Quoted message said:Subject: nicotine / nicotianamine From: [email hidden] (doe) Date: 10/3/2003 10:50 AM
Mountain Daylight Time Message-id: <[email hidden]>
Would anyone know whether nicotine is an iron chelator?
Planta. 2003 Jul;217(3):400-6. Epub 2003 Mar 15. Related Articles, Links
Discovery of an extended bundle sheath in Ricinus communis L. and its role as a temporal storage
compartment for the iron chelator nicotianamine.
Rutten T, Kruger C, Melzer M, Stephan UW, Hell R.
Institute of Plant Genetics and Crop Plant Research, Corrensstrasse 3, 06466, Gatersleben, Germany,
[email hidden]
The extended bundle sheath (EBS) is a specialized layer of cells that enhances the lateral
transport of photoassimilates within the leaf. This little-known tissue is often considered to be
legume-specific. We identified an EBS in cotyledons and leaves of the non-legume Ricinus communis
L. By means of cytological and immunological studies and using the localization of the
iron-chelator nicotianamine as an established indicator for mass transport, we confirmed its role
as a transport tissue and a temporal sink. Observations on cotyledons of Ricinus seedlings further
proved that the EBS carries out these tasks from a very early stage of development onwards. This is
the first time that information has been obtained on the physiological role of an EBS in a
non-legume. Our results support the idea of its widespread occurrence among higher plants.
PMID: 14520566 [PubMed - in process]
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<<snip>> reported capacity to prevent the Fenton reaction, probably by sequestration of
Fe2+, <<snip>>
Soto-Otero, R., E. Mendez-Alvarez, et al. (2002). "Effects of (-)-nicotine and (-)-cotinine on
6-hydroxydopamine-induced oxidative stress and neurotoxicity: relevance for Parkinson's disease."
Biochem Pharmacol 64(1): 125-35.
In view of the apparent controversial properties of (-)-nicotine (NIC) in relation to
both oxidative stress and neuroprotection, we studied the effects of NIC on hydroxyl
radical (*OH) formation, oxidative stress production by 6-hydroxydopamine (6-OHDA)
autoxidation in the presence and absence of ascorbate, and 6-OHDA neurotoxicity. Both
NIC and (-)-cotinine (COT) exhibited increased *OH production during 6-OHDA
autoxidation. Although the same effect was observed in *OH generation by the Fenton
reaction (H2O2 + Fe2+), this reaction was completely prevented with the previous
incubation of Fe2+ with NIC or COT. Furthermore, both NIC and COT demonstrated a
capacity to be able to reduce the TBARS formation provoked in rat brain mitochondrial
preparations by 6-OHDA autoxidation. This effect is assumed as a consequence of the
action of NIC and COT on lipid peroxidation propagation. We treated with NIC (1mg/kg,
i.p.) two 6-OHDA-induced rat models of Parkinson's disease. However, only in one of these models did
we obtain clear evidence of a neuroprotective effect of NIC on nigrostriatal terminals, as
revealed by immunohistochemistry against tyrosine hydroxylase. Thus, the antioxidant properties
of both NIC and COT in relation to the lipid peroxidation induced by 6-OHDA autoxidation,
together with their reported capacity to prevent the Fenton reaction, probably by sequestration
of Fe2+, may contribute to an understanding of its neuroprotective properties. In addition, the
reported capacity of both NIC and COT to increase the production of *OH by 6-OHDA autoxidation
might help explain the controversial observation found under different experimental conditions.
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