Biology Reference
In-Depth Information
observed, but gonads constitute a small proportion of whole-body RNA. A
reanalysis of these microarray data looking for up- or downregulated met-
abolic pathways found genes involved in increased fat usage and protein deg-
radation and decreased storage of fat, protein synthesis, and glucose
conversion to energy (
Zaya, Amini, Whitaker, & Ide, 2011
). These changes
correlate with morphological effects of atrazine, and could be due to a direct
effect of atrazine in these genes at the transcriptional level. Alternatively, the
authors suggested that atrazine may reduce food consumption thus indirectly
leading to altered gene regulation of metabolism genes. Detoxification of
atrazine is an energy intensive process and may place high demand for en-
ergy, perhaps an explanation for the etiology of atrazine's effects on slowed
growth and development. Reduced survivorship may be due to deleterious
effects on immune function perhaps leading to increased susceptibility to in-
fection. However, the cause of death was not determined. The role of al-
tered blood cell function in atrazine-treated tadpoles is not clear and
represents another example of microarray analysis revealing cryptic changes
not obvious from gross morphological or histological analysis. Different ef-
fects of atrazine observed between the sexes are not well understood.
3.2.3 PCBs
PCBs affect neural development, thereby implicating a potential role in TH
endocrine disruption based on TH's role in development of the nervous sys-
tem (
Jacobson & Jacobson, 1997
). Tadpole metamorphosis is used as a model
system to understand the role of PCBs on development to avoid the diffi-
culties of studying endocrine disruption in uterus-enclosed fetuses in mam-
mals. In tadpoles, hydroxylated polychlorinated biphenyls (OH-PCBs)
significantly delayed TH-induced metamorphosis (
Ishihara, Makita, &
Yamauchi, 2011
). Microarray on brain tissue showed that 526 TH-response
genes (25% of the 2139 T3-regulated genes) had altered TH responses in the
presence of 4-OH-PCB-106 and/or -159. GO categories significantly asso-
ciated with these genes were growth, brain development, cell proliferation,
cell adhesion, neuron differentiation, and apoptosis, providing molecular
underpinning of the presumed effects of PCBs on the tadpole brain. The fact
that most TH-response gene regulation was unaffected suggests that PCBs
may not act directly through TRs or that PCBs influence TRs only in a sub-
set of TH-response genes. The authors suggested the possibility that the 526
genes could be a source of biomarkers for PCB disruption of T3-dependent
brain development but did not characterize any.
