Application of Biodegradable Pesticides in India
289
in the experimental animals. Repeated oral, dennal, intraperitoneal, intravenous,
and intratesticular administration, alone or in combination with other insecticides,
produced varied toxicological effects (Datta, 1978; Datta and Dikshith, 1973,
1980; Dikshith, 1973, unpublished data; Dikshith et al., 1971; Dikshith and
Datta, 1972a,b, 1973).
Repeated oral feeding of endosulfan produced significant depletion of hepatic glycogen in male albino rats. The high activity of phosphorylase, hexokinase, aldolase, and succinate dehydrogenase suggested a rapid cycling of glycogenolysis, glycolysis, and Krebs cycle, respectively. There was no change in
the activity of fructose-l ,6-diphosphatase, but glucose-6-phosphatase showed a
significant increase which indicated a partial disturbance in gluconeogenesis.
Endosulfan also produced significant inhibition of glucose-6-phosphate dehydrogenase and lactate dehydrogenase, which in tum would block the HMP and
anaerobic glycolysis. The significant increase in the activity of ATPase suggested
the energy requirement for the metabolism of endosulfan-poisoned animals
(Kushwah and Dikshith, 1980; Dikshith et al., 1974, 1975a,b, 1976, 1978a-c,
1979, 1980a, unpublished; Gupta, 1976a,b; Gupta and Paul, 1974; Gupta and
Chandra, 1975; Kohli et al., 1974a,b; Kohli and Khanna, 1974; Anand et al.,
1977; Khanna et al., 1975; Matin, 1974; Matin and Kar, 1972, 1973, 1974;
Matin et al., 1976, 1977; Kar and Dikshith, 1970; Kar and Matin, 1971, 1972,
1974; Nath et al., 1978; Raizada et al., 1979, 1980; Kushwah and Dikshith,
1980).
Storage of endosulfan after repeated oral feeding for 30 days did not differ
significantly in the presence of metepa or otherwise. The highest level of residue
was observed in the kidney (6.5 ppm), while the lowest was in the blood (0.96
ppm). The observation did not suggest any kind of additive, antagonistic, or
potentiation effects of metepa and endosulfan in male rats (Nath et al., 1978).
Male and female rats, however, behaved in a different manner in the induction
of a toxic response (Dikshith et al., 1980a).
Skin painting rats with fenitrothion (0.1 ml of 95% purity) showed that the
insecticide is absorbed quickly through the skin, and a significant level was seen
in the blood within 2 hr after treatment. Insecticide level in the blood was
maximum after 8 hr and later showed a decrease. Inhibition of acetylcholinesterase after a single application of fenitrothion was 19.6% after three applications
it was 64.1%, and five applications produced total inhibition (Kohli et al.,
197 4a). Fenitrothion also caused loss of water from vital organs like the kidney,
brain, and heart. The spleen and brain also demonstrated maximum mobilization
of metals (Khanna et al., 1975).
Malathion (500 mglkg) administered through intraperitoneal injections produced a significant increase of blood glucose and plasma sodium and glycogen
of the liver, kidney, heart, and spleen of rats. There was a change in plasma
potassium and brain glycogen levels of treated rats (Gupta and Paul, 1974). Rats
289
in the experimental animals. Repeated oral, dennal, intraperitoneal, intravenous,
and intratesticular administration, alone or in combination with other insecticides,
produced varied toxicological effects (Datta, 1978; Datta and Dikshith, 1973,
1980; Dikshith, 1973, unpublished data; Dikshith et al., 1971; Dikshith and
Datta, 1972a,b, 1973).
Repeated oral feeding of endosulfan produced significant depletion of hepatic glycogen in male albino rats. The high activity of phosphorylase, hexokinase, aldolase, and succinate dehydrogenase suggested a rapid cycling of glycogenolysis, glycolysis, and Krebs cycle, respectively. There was no change in
the activity of fructose-l ,6-diphosphatase, but glucose-6-phosphatase showed a
significant increase which indicated a partial disturbance in gluconeogenesis.
Endosulfan also produced significant inhibition of glucose-6-phosphate dehydrogenase and lactate dehydrogenase, which in tum would block the HMP and
anaerobic glycolysis. The significant increase in the activity of ATPase suggested
the energy requirement for the metabolism of endosulfan-poisoned animals
(Kushwah and Dikshith, 1980; Dikshith et al., 1974, 1975a,b, 1976, 1978a-c,
1979, 1980a, unpublished; Gupta, 1976a,b; Gupta and Paul, 1974; Gupta and
Chandra, 1975; Kohli et al., 1974a,b; Kohli and Khanna, 1974; Anand et al.,
1977; Khanna et al., 1975; Matin, 1974; Matin and Kar, 1972, 1973, 1974;
Matin et al., 1976, 1977; Kar and Dikshith, 1970; Kar and Matin, 1971, 1972,
1974; Nath et al., 1978; Raizada et al., 1979, 1980; Kushwah and Dikshith,
1980).
Storage of endosulfan after repeated oral feeding for 30 days did not differ
significantly in the presence of metepa or otherwise. The highest level of residue
was observed in the kidney (6.5 ppm), while the lowest was in the blood (0.96
ppm). The observation did not suggest any kind of additive, antagonistic, or
potentiation effects of metepa and endosulfan in male rats (Nath et al., 1978).
Male and female rats, however, behaved in a different manner in the induction
of a toxic response (Dikshith et al., 1980a).
Skin painting rats with fenitrothion (0.1 ml of 95% purity) showed that the
insecticide is absorbed quickly through the skin, and a significant level was seen
in the blood within 2 hr after treatment. Insecticide level in the blood was
maximum after 8 hr and later showed a decrease. Inhibition of acetylcholinesterase after a single application of fenitrothion was 19.6% after three applications
it was 64.1%, and five applications produced total inhibition (Kohli et al.,
197 4a). Fenitrothion also caused loss of water from vital organs like the kidney,
brain, and heart. The spleen and brain also demonstrated maximum mobilization
of metals (Khanna et al., 1975).
Malathion (500 mglkg) administered through intraperitoneal injections produced a significant increase of blood glucose and plasma sodium and glycogen
of the liver, kidney, heart, and spleen of rats. There was a change in plasma
potassium and brain glycogen levels of treated rats (Gupta and Paul, 1974). Rats