ISSN
1916-6958

2010;
Volume 1 (Number 2): Pages 37-38

EDITORIAL

In this issue: four outstanding scientific
contributions to the journal in the form of review papers and original studies
in experimental animal models

Alejandro A. NAVA-OCAMPOa,b

aPharmaReasons, Toronto ON, Canada

bDepartment of Pharmacology & Toxicology, Faculty
of Medicine, University of Toronto, Toronto ON, Canada

Correspondence:
[email-masked]

In
this second number of the first volume of the journal, we have selected two
review papers and two original studies for publication.

Doxorubicin
(DOX) is an anthracycline antibiotic discovered and isolated from Streptomyces peucetius several decades
ago. It still remains as one of the most important antineoplastic agents used
against a broad spectrum of cancer. The anticancer activity of DOX is
attributable to its ability to bind and intercalate the DNA double strand
causing a stereochemical disorder and thus inhibiting the synthesis of DNA,
RNA, and proteins, eventually leading to cell death.

The
review by PEREIRA & OLIVEIRA [1] summarized the current knowledge on the mitochondrial
targets of DOX toxicity as well as the pharmacological strategies designed to
decrease it. The authors reviewed the effects of DOX on mitochondrial
physiology and bioenergetics as well as the consequences at the myocyte level,
the non-pharmacological strategies already demonstrated to counteract
DOX-induced cardiotoxicity, and the damage-preventing approaches involving
mitochondria and their mechanism. The manuscript contains an in-depth analysis
of the topic that the readers may find helpful for developing new strategies to
counteract DOX toxicity focusing on the mitochondria as the target.

Persistent
pulmonary hypertension of the neonate significantly contributes to an increase
of neonatal morbidity and mortality, including asphyxia during delivery,
meconium aspiration, and respiratory distress syndrome. In the review paper by
GONZÁLEZ-LOZANO et al. [2], the evaluation of pulmonary vasodilators in animal
models as well as in some clinical trials was reviewed. The authors concluded
that experimental animal models are critical for examining, in depth, current
pharmacological alternatives for treating human babies as well as for
developing new therapeutic options. However, as with any experimental animal
model, interspecies differences should be considered when evaluating the
mechanisms involved in perinatal asphyxia, its consequences and treatment.

Regarding
drug therapy, inhaled nitric oxide (iNO) remains as the pulmonary vasodilator
of choice in neonates with pulmonary hypertension. However, sildenafil, an
non-specific inhibitor of type-5 phosphodiesterases (5-PDE) that enhances the
vasodilatory effects of nitric oxide by decreasing the biodegradation of a
second-messenger GMPc, has shown to be a good alternative both as a single drug
or associated with iNO.

Cocaine
addiction has been a serious medical and social problem in recent years and
intensive research has been carried out in an attempt to explain the behavioral
and neurobiological bases of its development. In this context, studies in
experimental animal models to investigate the neurobehavioral consequences of
cocaine discontinuation are fundamental to understand the mechanisms involved
in addiction and craving.

GOMES
SILVA et al. [3] evaluated animals treated
once a day, during a week, with cocaine 20 mg kg-1 or saline
(control), intraperitoneally. Following one or seven days of cocaine
administration, animals were submitted to the forced swimming (FST) and open
field tests (OFT), while another group of animals was decapitated and their
brain striatum was removed for determination of dopamine (DA) and serotonin
(5-HT) and their metabolites levels. Interestingly, the authors found evidence
to indicate that one or seven days of cocaine administration in rats, at low
doses, was not enough to produce symptoms of depression.

Ischemia
of central nervous system is associated with increased extracellular
concentrations of glutamate, which leads to uncontrolled activation of NMDA
receptors and favors the influx of calcium. Glycine is an inhibitory
neurotransmitter amino acid that acts as neuromodulator of NNMDA receptors,
critically involved in the process of ischemic brain injury. URIBE-ESCAMILLA
et al. [4] investigated the potential
neuroprotective effects of glycine in an experimental animal model of ischemic
brain damage.

The
authors concluded that glycine administered i.p. to rats with permanent left
carotid occlusion limited the ischemic brain damage, probably by increasing the
neurological availability of glycine concentration enough to prevent the
desensitization of NMDA receptors and consequently altering the cascade of
events that lead to cellular death. However, levels of glycine have been associated
with the severity of hypoxic encephalopathy-ischemic observed in human infants
and further studies to clarify the neuroprotective role of glycine are
warranted.

The
issue of the journal is a continuation of our original plan to publish relevant
studies and to be among the best options for journals covering the topics found
in the Journal of Theoretical & Experimental
Pharmacology. Although a substantial effort has been made to expedite the
review and publication processes, we are still facing some tough challenges
that have required the dedicated effort of numerous people. Although these
challenges appear to be enormous, the support provided by the Editorial Board
is encouraging and has facilitated the work of the supporting team.

As
always, I would like to express my gratitude to the authors of the published
manuscripts for giving us the opportunity to publish their studies in this
journal, and to the readers for using the journal as a source of information.

The
Editor

REFERENCES

[1]
Pereira GC,
Oliveira PJ. Pharmacological strategies to counteract doxorubicin-induced
cardiotoxicity: the role of mitochondria. J Theor Exp Pharmacol 2010; 1: 39-53.

[2]
González-Lozano
M, Nava-Ocampo AA, Trujillo-Ortega ME, Alonso-Spilsbury M, Mota-Rojas D. A
critical overview of clinical and experimental studies on pulmonary
vasodilators in newborns. J Theor Exp Pharmacol 2010; 1: 54-61.

[3]
Gomes Silva MI, De Oliveira Citó MC,
Falcão do Amaral J, De Aquino Neto MR, Arcanjo Moura B, Freire de
Vasconcelos P, et al. Behavioral
and neurochemical evaluation in rats withdrawn from repeated cocaine treatment
and exposed to the forced swimming and open field tests. J Theor Exp Pharmacol
2010; 1: 62-71.

[4]
Uribe-Escamilla R, Padilla-Martín K,
González-Maciel A, Arch-Tirado E, Nava-Ocampo AA,
Alfaro-Rodríguez A. Neuroprotective effects of glycine in rats with
permanent cerebral ischemia. J
Theor Exp Pharmacol 2010; 1: 72-75.

www.premiumreasons.com/JTEP/JTEP.html

© PremiumReasons