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Pregnant Swiss albino rats were divided into three groups: control (C), gestational exposure of Cd (G-Cd), and gestational/postnatal exposure of Cd (GP-Cd) groups. Control animals received tap water, and the rats of GP-Cd group received Cd as CdC12 in their drinking water during the experimental period. The G-Cd group was given Cd during pregnancy, but given tap water after birth. Twenty-two days after birth, 15 rats (for each group) were taken from their mothers and continued to be treated with Cd (GP-Cd group) or tap water (C and G-Cd groups) for an additional 38 days. On postnatal day (PND) 60, flash visual evoked potentials (FVEPs) were recorded with disc electrodes attached with collodion 0.5 cm in front of and behind bregma. The mean latencies on N1, P2, and P3 were prolonged in the GP-Cd group compared with controls. The mean latency of P3 was also significantly different between G-Cd and GP-Cd groups. P1-N1 and N1-P2 amplitudes of VEPs were significantly decreased in the GP-Cd group compared with control group. N1-P2 amplitude of the G-Cd group was significantly lower than that of the control group. Thiobarbituric acid reactive substances (TBARS) were determined as an indicator of lipid peroxidation. Our data showed that pre- and postnatal Cd treatment caused a significant increase of lipid peroxidation in the brain.
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July 2005,
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association,
P Yargiçoğlu, and
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January 2000,
The International journal of neuroscience,
P Yargiçoğlu, and
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December 2007,
Brain research,
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August 1971,
Brain research,
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January 2011,
Neurotoxicology and teratology,
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January 2018,
Noro psikiyatri arsivi,
P Yargiçoğlu, and
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June 1997,
International journal of leprosy and other mycobacterial diseases : official organ of the International Leprosy Association,
P Yargiçoğlu, and
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July 2013,
International journal of psychophysiology : official journal of the International Organization of Psychophysiology,
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January 1993,
Nihon seirigaku zasshi. Journal of the Physiological Society of Japan,
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January 1995,
Alzheimer disease and associated disorders,
