Testicular Atrophy in Gallus domesticus Fed Acute Doses of Copper Fungicides

Abstract

Acute oral toxicity of the copper fungicides, copper sulphate and copper oxychloride, were studied in male Gallus domesticus. The median lethal dose for copper sulphate and copper oxychloride determined were 693 and 1263 mg/kg body weight, respectively. Severe diarrhea and delayed mortality (3 to 6 days) was characteristic of copper oxychloride. Liver weights were nearly doubled in birds fed copper oxychloride and marked dose-dependent testicular atrophy was noticed in both copper sulphate and copper oxychloride fed birds. Mild to severe spermatogenetic arrest concomitant with testicular atrophy was observed. Histochemically, the interstitial (Leydig) cells and seminiferous tubules showed intense accumulation of cholesterol-positive lipids. The degree of lipophilia appeared to be directly proportional to the extent of spermatogenetic arrest, and these results are suggestive of steroidogenic inhibition in the Leydig cells of the atrophied testis.

Ingestion of bedding material as a cause of acute copper sulfate poisoning in turkey poults

“…In our case, surface erosions and ulceration of the mucous membrane of the gizzards as well as liver congestion were observed in all examined birds. Our findings concur well with the results of an experiment on White Leghorn males fed with acute doses of 2 Cu compounds (Shivanandappa et al, 1983). The authors described the impairment of spermatogenesis concomitant with testicular atrophy, congestion of the liver and kidneys and high mortality that occurred within 24 to 28 h in birds fed with CuSO 4 .…”

Postnatal toxicity of copper oxychloride in lactating female albino rats

“…For the hematological findings, all lactating dams treated with different doses of COC (147 and 73.5 mg/kg Bw. COC) showed that there was a significant decrease in RBCs count, Hb content and PCV in all treated dams with elevation in leukocytic counts and as well [9] reported that copper oxychloride may accumulate in various tissues as a heavy metal and cause hemolytic anemia, also [26] found that copper may promote hemolysis anemia and hemorrhage with abnormal high blood Cu+ levels . However, the elevation of the leukocyte counts considered as a precise indicator of the immune system, defense mechanism and increase in the inflammatory response upon exposure to environmental pollutant and pesticides [27].…”

Copper and copper containing pesticide as copper oxychloride toxicity and its adverse effects on animal and human health

“…Furthermore, COC confirmed to inhibit spermatogenesis and affect the function of leydig cells with steroidogenic inhibition and cholesterol accumulation in such cells, such reproductive toxic effect may be due to Cu+ capability of interaction with other metals as selenium, iron and zinc and in turn affect their absorption through antagonism resulted in a deficiency of such element with subsequent cellular dysfunction with deleterious effect on the testes (19,27) The toxic effect of copper on the follicular waves also observed in female mouse ovaries (intraperitoneal injection of 70mg/ kg of CuCl2in adult female mice) and the results revealed a significant increase in stage II follicles with degeneration and apoptosis of oocytes and oocyte fragmentation in treated groups than control (39) even in earthworm Eisenia fetida the cocoon production and hatchling were significantly reduced upon exposure for different concentrations of copper oxychloride (40).…”

“…Copper is considered an essential micronutrient and many animals can cope with excess copper exposure by the liver but the overwhelming of such mechanism may occur with repeated exposure (15) resulting in hemolysis, anemia, diarrhea, hemorrhage, kidney failure, and death of animals (19).…”