Pesticides can cause gene mutations and chromosomal aberrations in exposed individuals. We have investigated 24 workers exposed to pesticides. Clinical examinations and cytogenetic and toxicological tests were performed. Ten non-exposed individuals were used as controls. Toxicological dosages of copper, zinc and manganese (metals found in some pesticides), hepatic enzyme dosage (GOT, GPT, AR) and acetylcholinesterase activity were performed in 16 workers and 8 controls. In the exposed workers, the most relevant clinical symptoms were poor digestion with fullness sensation after meals, irritated eyes, headache and fasciculations. The exposed group showed significantly lower manganese dosage and acetylcholinesterase activity, and significantly higher levels of alkaline phosphatase. Cytogenetic studies showed significantly higher chromosomal aberrations in the exposed group compared to the control group. Although the workers used protection against the pesticide's fog, the results revealed that the workers were contaminated with the pesticides. Therefore, the cytogenetic, toxicological studies with clinical examination are necessary for monitoring workers who are exposed to pesticides in any situation.
Prostate cancer (PCa) is the most commonly diagnosed cancer in men. The etiology of PCa in humans is multifactorial and includes age, ethnicity, environmental factors, and other unknown causes. Epidemiological and experimental evidence has shown that cadmium is associated with PCa both in humans and rodents. This metal can act as an endocrine disruptor during prostate development, and it induces prostate lesions late in life. In this study, we investigated the effects of low-dose cadmium on rat prostate morphology during puberty. Two-month-old male Wistar rats were randomized into two experimental groups: cadmium-treated and control. The ventral and dorsolateral prostates were dissected, weighed, and immunohistochemically stained with specific antibodies against Ki-67 and the androgen receptor (AR). The concentration of cadmium was measured in the blood and prostate, and testosterone concentration was measured from the plasma. Our results show that cadmium concentration was increased in both the blood and the prostate of cadmium-treated rats, but there were no changes in the prostatic weight, epithelial cell height, or testosterone levels. However, AR immunostaining and epithelial cell proliferation (Ki-67 index) were increased in both prostates with an increase in apoptosis only in the dorsal lobe. Furthermore, atypical hyperplasic proliferative lesions were found in the dorsolateral lobe after cadmium exposure. Cadmium treatment reduced collagen fiber absolute volume in both prostates. Thus, low-doses of cadmium, even for a short period of time, can interfere with prostate epithelium-stroma homeostasis, and this disruption might be an important factor in the onset of prostate lesions late in life.
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