Quoted message said:Subject: nicotine / nicotianamine
From: [email hidden] (doe)
Date: 10/3/2003 10:51 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.
Who loves ya.
Tom
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