Page 39 - Msingi Afrika Magazine Issue 11

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such as ERK1/2 and p38MAPK all
play a role in eliciting Ca2+ influx
and cell death.

Roundup also decreases the levels
of reduced glutathione (GSH, the
tissue’s own antioxidant) as con-
sistent with oxidative stress, and
increases the amounts of thiobarbi-
turic acid reactive species (TBARS)
and protein carbonyls, which are
signs of oxidative damage from
reactive oxygen species to lipids and
proteins respectively. Exposure to
Roundup stimulates the activities
of a whole collection of enzymes There is already evidence that oxidative stress attacks the lipids of
supporting the down-regulation of glyphosate may act as an endocrine the sperm plasma membrane and
GSH levels. disruptor for both males and fe- the integrity of DNA in the sperm
males by altering aromatase activity, nucleus. In addition, ROS induce
The research team looked at acute oestrogen regulated genes, and DNA damage, accelerate germ cell
Roundup exposure of both whole testosterone levels in rats [10]. But death and decrease sperm counts,
immature Wistar rat testis and iso- Roundup acts via different mech- thereby contributing to male infer-
lated Sertoli cells in culture; and the anisms. Roundup exposure during tility.
findings were very similar in the two pregnancy and lactation at a level
systems. that did not induce maternal toxicity ROS is so closely linked to male
in Wistar rats nevertheless induced infertility that infertile males gener-
Based on their experimental results, adverse reproductive effects in male ating high levels of ROS are 7 times
the team propose that Roundup offspring, including decreased daily less likely to initiate a pregnancy
toxicity is due to Ca2+ overload, re- sperm production during adulthood, compared with those with low levels
sulting in cell signalling fault, a stress increase in abnormal sperms, and of ROS. A meta-analysis demon-
response and/or defence against low testosterone serum level at pu- strated that ROS levels were signifi-
depleted antioxidant, all contributing berty. In exposed female offspring, cantly correlated with the fertiliza-
to the death of Sertoli cells, thereby only a delay in vaginal canal opening tion rate in couples undergoing in
impacting on male fertility. was observed [11]. vitro fertilization [16].

The new findings are consistent Oxidative stress and en- Ashok Agarwal at the Center for
with the well-known involvement of Advanced Research in Human
Ca2+ in cell death from oxidative docrine disrupting effects Reproduction, Infertility and Sexual
stress. Oxidative stress causes Ca2+ specific to Roundup Function, Cleveland Ohio in the
influx into the cytoplasm from The key to understanding the action United States led a retrospective
the extracellular environment and of Roundup on male infertility is study on 132 male factor infertility
from the endoplasmic reticulum [9]. the reactive oxygen species (ROS) (MFI) patients (failure to initiate
Rising Ca2+ concentration in the generated in oxidative stress (see pregnancy with fertile partner after
cytoplasm in turn causes Ca2+influx [12, 13] The Body Does Burn Water one year of unprotected sex) con-
into the mitochondria and nuclei. In and Living with Oxygen, SiS 43). sisting of 24 with all normal sperm
the mitochondria, Ca2+ accelerates Not only are ROS implicated in parameters, 38 with all abnormal pa-
the disruption of normal oxidative practically every chronic human dis- rameter and the rest with 1 or more
metabolism leading to necrotic cell ease including cancer [14] (Cancer a abnormal parameters [17]. They
death. In nuclei, Ca2+ modulates Redox Disease, SiS 54), but also play found that the 34 normal healthy
gene transcription and nucleases an essential role in the pathogenesis donors (controls) had significant-
that control apoptosis (programmed of many reproductive processes as ly higher sperm concentrations,
cell death that involves fragmenta- detailed in a review published in motility and morphology compared
tion of DNA). 2003 [15]. In male-factor infertility,

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